Rapid Responses to:
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Rapid Responses: Rapid Responses published:
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Inexpensive and Highly Effective Nutritional Management of Atopic Dermatitis
- Joseph M Mercola (28 June 2002)
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Resolution of atopic dermatitis with gliaden-free and casein-free diet
- Pauline A. Harding, M.D. (12 July 2002)
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New Treatments for Atopic Dermatitis
- B.Roger Allen, Thomas A luger (9 August 2002)
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Potential conflict of interests
- Hywel C Williams (12 August 2002)
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Joseph M Mercola, Medical Director Optimal Wellness Center Schaumburg, IL 60194
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While Dr. Williams does an excellent job in reviewing some of the newer pharmacologically based approaches to atopic dermatitis, it is most disappointing that the review fails to acknowledge the new advances in inexpensive, non-toxic, highly effective and widely available tools of nutritional management for this common problem. Over the last 15 years our center has routinely provided resolution of severe cases of atopic dermatitis with inexpensive nutritional manipulations that are not covered in this review. These dietary changes have had profound beneficial effects in the most extreme cases of atopic dermatitis we have seen. The key is balancing the omega 6:3 fat ratio. The first step is a severe limitation of n-6 fats that are converted to inflammatory archidonic acid lipoxygenase mediators. N-6 fats are common in nearly all polyunsaturated vegetable oil products (with the exclusion of olive and canola oils, which are relatively high in n-9 and n-3 fats respectively). Bakery products are particularly troublesome, as high percentages of the n -6 fats have been converted to trans isomers that further exacerbate the dermatitis. The second step would be to increase elongated n-3 fats, such as EPA and DHA that are common in fish oils. Cod liver oil is profoundly effective here as it has significant quantities of vitamin D and vitamin A that frequently provide synergistic therapeutic effects. Typical daily therapeutic quantities of n-3 fats are 300 mg per 4 kg of body weight. Supplementation with the shorter chain n-3 fat, ALA (i.e. flax) is frequently not sufficient to generate significant quantities of beneficial eicosanoids as only 10% of ALA is elongated and desaturated to the higher chain n-3 fats, EPA and DHA. If the child is breast-fed these dietary manipulations are, of course, initiated through the nursing mother. If the child is eating table foods two additional manipulations are most useful. The first is to limit most grains and fruit juices as they are rapidly converted to simple carbohydrates that increase insulin levels. The increased insulin levels inhibit delta-6 desaturase, which converts linoleic acid to gamma- linolenic acid (GLA). The elevated insulin levels also facilitate delta-5 desaturase, which further increases pro- inflammatory by products of arachidonic acid. Although GLA is an n-6 fat, we frequently find supplements of 2-3 gram quantities GLA from evening primrose oil beneficial in compensating for the impaired delta-6 desaturase activity. Additionally, restriction of all gluten and casein containing foods and regular exposure to sun provide additional valuable measures in healing this challenging problem. References Mayser P, Mayer K, Mahloudjian M, A double-blind, randomized, placebo -controlled trial of n-3 versus n-6 fatty acid-based lipid infusion in atopic dermatitis. JPEN J Parenter Enteral Nutr. 2002 May-Jun;26(3):151-8. Reynolds, NJ, et. al. Narrow-band ultraviolet B and broad-band ultraviolet A phototherapy in adult atopic eczema: a randomised controlled trial. Lancet June 23, 2001; 357: 2012-16 Solvoll K, Soyland E, Sandstad B, Dietary habits among patients with atopic dermatitis. Eur J Clin Nutr. 2000 Feb;54(2):93-7. Yu G, Bjorksten B. Polyunsaturated fatty acids in school children in relation to allergy and serum IgE levels. Pediatr Allergy Immunol. 1998 Aug;9(3):133-8. |
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Pauline A. Harding, M.D., Lecturer, University of Illinois College of Medicine Medical Director,Wellness Innovations Network 27W281 Geneva Road, Suite D, Winfield IL 60190-2037
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Dr. Williams'review of the management of atopic dermatitis focuses on the pharmacologic approaches. The pathophysiologic mechanisms involved in atopic dermatitis also dictate attention to the nutritional and dietary components of management. Skin regeneration and healing is disrupted by elevated levels of secretory cortisol, especially elevated nocturnal levels. These disruptions in the circadian rhythm of cortisol are induced by skipping meals,ingestion of excess sugars and starches, failure to eat low-glycemic index foods every 5 hours while awake, ingestion of foods which cause inflammatory reactions in the gut (e.g., casein-containing dairy products and gliaden-containing grain products), pain, emotional stress, and late bedtimes. The elevated cortisol secretion can be offset by control of hyperinsulinemia (by glycemic balancing of each meal), avoidance of gliaden and casein in the diet of the child (and in the diet of the mother if the infant is nursing), and avoidance of late evening snacks, especially carbohydrates. Oral administration of phosphatidyl serine (in the late afternoon or early evening)counteracts the nocturnal cortisol elevation in some individuals. Oral supplementation with essential fatty acids (especially omega-3 oils)and zinc citrate or zinc gluconate also promote the healing of skin. |
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B.Roger Allen, Consultant Dermatologist University Hospital Nottingham NG7 2UH, Thomas A luger
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Dear Sir As clinicians who have been involved in the clinical development of the two drugs (tacrolimus and pimecrolimus) which are the main focus of Prof Williams’ editorial 29 June (BMJ 324; 1533-4), we feel that its somewhat negative nature deserves comment. It is an almost unbelievable 50 years since the last innovative breakthrough in the topical treatment of atopic dermatitis - the development of corticosteroids - and we have every reason to be excited at the prospects these new entities offer. Prof Williams unreservedly acknowledges that their efficacy has been proved but from then onwards the editorial totally lacked any patient perspective. The issue lies not in disembodied comparisons of efficacy from the clinicians point of view but which treatment provides the most acceptable benefit / risk ratio from the patients position or, in the case of children, that of their parents. Work from Prof Williams own department (1), has shown that, in many cases, from the patients’ perspective using a corticosteroid to control their eczema produces risks which are unacceptably high, resulting in non- compliance and inadequate treatment. These findings are further supported by a US study which showed that only 40% of AD patients were satisfied with their treatment (2). The main fear which patients had was of skin thinning, a risk which has been completely eliminated with these new therapies. Far from being ‘rare’ the risks of adverse events from using steroids are directly related to the duration and quantity of use and the potency of the steroid applied so todays patients are just as much at risk as before unless they choose to endure the misery of their condition and leave it under treated. Patients’ fears about steroids can hardly be dismissed as ‘irrational’ even though they may be exaggerated. Topical tacrolimus and pimecrolimus offer a realistic reduced-risk alternative of proven efficacy whatever their potencies relative to corticosteroids. Prof Williams invites us to use our imagination as to which of the two is the more effective. This would hardly be evidence based and with experience of both we decline to do so since it would overlook the differences in indictions, formulations and pharmacology of the two structurally-similar drugs. It has never been suggested that just one topical steroid would be appropriate for all purposes and the same applies to these topical calcineurin inhibitors. Although the editorial declares the use of probiotics harmless the long-term risks of such strategies is currently unknown and the subject of debate (3) and their safety has not been tested on anything like the 13,000 included in the trials of tacrolimus and pimecrolimus. Of course, as with any new therapy, close monitoring over the coming years will be mandatory but in addition to the short-term safety of these drugs, which are mentioned in the editorial, longer-term studies with pimecrolimus (4) and tacrolimus (5) show no clinically significant increase in any infections or skin cancers. Since the drugs are non- mutagenic and do not permanently impair primary immune responses, an increased risk of skin cancer is most unlikely. Suggesting a risk of visceral cancer from the topical use of these non-mutagenic drugs which are absorbed to a near negligible degree must surely count as scaremongering. It is of note that with over 40 years of use of potent topical steroids which not only deplete cutaneous Langerhans cells but are highly immunosuppressant as well as being systemically absorbed there is no evidence that they predispose to cancer either cutaneous or systemic. These new treatments for atopic dermatitis are welcomed by patients, parents of patients, and physicians including dermatologists and pediatricians, as another treatment option for this demoralising disease, and the first major advance in its management in half a century. 1. Charman CR, Morris AD, Williams HC. Topical corticosteroid phobia in patients with atopic eczema. Br J. Derm 2000; 142: 931-36. 2. Hanifin J, McAlister RO, Tofte S. Perspectives on atopic dermatitis: The patients’ and physicians’ point of view. Poster #105 at 58th Annual Meeting of the American Academy of Dermatology, March10-15, 2000. 3. Murch SH Toll of allergy reduced by probiotics (commentary) Lancet 2001;357:1057-1058 4. Wahn U, Bos JD, Goodfield M, Caputo R, Papp K, Manjra A, Dobozy A, Paul C, Molloy S, Hultsch T, Graeber M, Cherill R, de Prost Y. Efficacy and safety of pimecrolimus cream in the long-term management of atopic dermatitis in children. Pediatrics 2002;110:1–8 5. Kang S, Lucky AW, Pariser D, Lawrence I, Hanifin JM. Long-term safety and efficacy of tacrolimus ointment for the treatment of atopic dermatitis in children. J Am Acad Dermatol 2001; 44 (1 Suppl): S58-64 B.Roger Allen
Thomas A Luger
(Both authors have received funding from Fujisawa and Novartis to carry out clinical studies on tacrolimus and pimecrolimus) |
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Hywel C Williams, Professor of Dermato-Epidemiology University of Nottingham, NG7 2UH
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I would like to thank those that have written in response to my editorial which was intended to draw attention to some of the unanswered questions regarding new treatments for atopic dermatitis. I have not responded to the rapid responses of Drs. Mercola and Harding as both have made excellent contributions to bringing our attention to other non-pharmacological approaches for atopic dermatitis - a point which, perhaps, I did not make strongly enough in the editorial. Dr. Allen and Prof Luger give us a robust promotion of topical tacrolimus and pimecrolimus. Before I respond to their thoughtful comments, please could the authors provide us details of the full extent of their potential conflicts of interest here. In addition to receiving research monies for helping to develop these products, has either author in the last 5 years i) received an honorarium or speakers fee for talking at a meeting sponsored by Novartis or Fujisawa? ii) received a fee for writing "educational" articles in magazines directly or indirectly sponsored by Fujisawa or Novartis? iii) received any money as an advisor or consultant to Novartis or Fujisawa? iv) been reimbursed by these two companies for attending a symposium? v) received a fee for organising education? vi) received funds for a member of staff? vii) held any stocks or shares relating to the two companies concerned? I am not suggesting for a moment that their response has anything to do with their possible ties to the two companies concerned, but nevertheless I think it is important that those potential ties are declared fully in the public domain in order to make a judgement. There is no need to disclose the amounts of monies involved - just simple yes/no answers please. Thank you |
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