Docosahexaenoic acid (DHA) supplementation in atopic eczema: a randomized, double-blind, controlled trial

Koch, Christin; Dölle, Sabine; Metzger, Manuel; Rasche, Claudia; Jungclas, H.; Rühl, Ralph; Renz, Harald; Worm, Margitta

doi:10.1111/j.1365-2133.2007.08430.x

Cited by 78 publications

(67 citation statements)

References 36 publications

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“…In a recent clinical trial, we showed that high dose DHA supplementation improves the clinical outcome of atopic eczema and causes a prominent inhibition of anti-CD40/IL-4 stimulated IgE production in PBMC ex vivo [31]. These data prompted us to investigate the underlying molecular mechanisms of DHA action on B cells.…”

Section: Introductionmentioning

confidence: 97%

Inhibition of IgE production by docosahexaenoic acid is mediated by direct interference with STAT6 and NFκB pathway in human B cells

Weise

Hilt

Milovanović

et al. 2011

The Journal of Nutritional Biochemistry

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Section: Introductionmentioning

confidence: 97%

Inhibition of IgE production by docosahexaenoic acid is mediated by direct interference with STAT6 and NFκB pathway in human B cells

Weise

Hilt

Milovanović

et al. 2011

The Journal of Nutritional Biochemistry

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“…Evidence supporting an enhanced consumption of long-chain n-3 PUFAs includes a study in which children with atopic eczema were found to have lower serum levels of EPA and DHA than non-atopic children, despite similar levels of fish consumption [2]. Results from intervention studies have been inconclusive [13][14][15]. Various animal models have been used to study the role of n-3 PUFAs in atopic inflammation.…”

Section: Introductionmentioning

confidence: 99%

Long-chain polyunsaturated fatty acids are consumed during allergic inflammation and affect T helper type 1 (Th1)- and Th2-mediated hypersensitivity differently

Johansson

Lönnqvist

Östman

et al. 2010

Clinical and Experimental Immunology

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SummaryStudies have shown that atopic individuals have decreased serum levels of n-3 fatty acids. Indicating these compounds may have a protective effect against allergic reaction and/or are consumed during inflammation. This study investigated whether fish (n-3) or sunflower (n-6) oil supplementation affected T helper type 1 (Th1)-and Th2-mediated hypersensitivity in the skin and airways, respectively, and whether the fatty acid serum profile changed during the inflammatory response. Mice were fed regular chow, chow + 10% fish oil or chow + 10% sunflower oil. Mice were immunized with ovalbumin (OVA) resolved in Th1 or Th2 adjuvant. For Th1 hypersensitivity, mice were challenged with OVA in the footpad. Footpad swelling, OVA-induced lymphocyte proliferation and cytokine production in the draining lymph node were evaluated. In the airway hypersensitivity model (Th2), mice were challenged intranasally with OVA and the resulting serum immunoglobulin (Ig)E and eosinophilic lung infiltration were measured. In the Th1 model, OVA-specific T cells proliferated less and produced less interferon (IFN)-g, tumour necrosis factor (TNF) and interleukin (IL)-6 in fish oil-fed mice versus controls. Footpad swelling was reduced marginally. In contrast, mice fed fish oil in the Th2 model produced more OVA-specific IgE and had slightly higher proportions of eosinophils in lung infiltrate. A significant fall in serum levels of long-chain n-3 fatty acids accompanied challenge and Th2-mediated inflammation in Th2 model. Fish oil supplementation affects Th1 and Th2 immune responses conversely; significant consumption of n-3 fatty acids occurs during Th2-driven inflammation. The latter observation may explain the association between Th2-mediated inflammation and low serum levels of n-3 fatty acids.

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“…In a pilot study, the latter group also tested the therapeutic effect of DHA in adult patients with atopic dermatitis: after eight weeks, daily administration of 5.4 g DHA led to marked improvement in the skin condition, a rise in n-3 FA plasma levels, and an improved n-6:n-3 ratio [41]. In this study, too, IgE synthesis was suppressed by DHA ex vivo.…”

Section: Prospects For Treatmentmentioning

confidence: 80%

Do long‐chain omega‐3 fatty acids protect from atopic dermatitis?

Reese

Werfel

2015

J Deutsche Derma Gesell

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Summary Long‐chain polyunsaturated fatty acids are essential for human nutrition. The number of double bonds determines whether a given fatty acid is termed two, three, or x times unsaturated. Depending on the distance of the first double bond from the fatty acid's methyl group, one distinguishes omega‐3 fatty acids from omega‐6 fatty acids. While the use of gamma linolenic acid, a long‐chain fatty acid of the omega‐6 family, has proven unsuccessful in the prevention or treatment of atopic dermatitis, supplementation of long‐chain omega‐3 fatty acids may represent a promising approach in the prevention of allergic disorders, especially atopic dermatitis. Whether the concept of long‐chain omega‐3 fatty acid administration will also become established in a therapeutic setting, depends on whether the beneficial effects observed so far can be substantiated in randomized controlled intervention studies.

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Docosahexaenoic acid (DHA) supplementation in atopic eczema: a randomized, double-blind, controlled trial

Abstract: Our data suggest that dietary DHA could be bioactive and might have a beneficial impact on the outcome of atopic eczema, but our results need to be confirmed in a larger study.

Cited by 78 publications

References 36 publications

Inhibition of IgE production by docosahexaenoic acid is mediated by direct interference with STAT6 and NFκB pathway in human B cells

Inhibition of IgE production by docosahexaenoic acid is mediated by direct interference with STAT6 and NFκB pathway in human B cells

Long-chain polyunsaturated fatty acids are consumed during allergic inflammation and affect T helper type 1 (Th1)- and Th2-mediated hypersensitivity differently

Do long‐chain omega‐3 fatty acids protect from atopic dermatitis?

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