Revisiting the Dutch hypothesis.
The Dutch hypothesis was first articulated in 1961, when many novel and advanced scientific techniques were not available, such as genomics techniques for pinpointing genes, gene expression, lipid and protein profiles, and the microbiome. In addition, computed tomographic scans and advanced analysis techniques to dissect (small) airways disease and emphysema were not available. At that time, the group of researchers under the visionary guidance of Professor N. G. M. Orie put forward that both genetic and environmental factors can determine whether one would have airway obstructive diseases, such as asthma and chronic obstructive pulmonary disease (COPD). Moreover, they stipulated that the phenotype of obstructive airway disease could be affected by sex and changes with aging. Orie and colleagues' call to carefully phenotype patients with obstructive airways diseases has been adopted by many current researchers in an attempt to determine the heterogeneity of both asthma and COPD to better define these diseases and optimize their treatment. The founders of the Dutch hypothesis were far ahead of their time, and we can learn from their insights. We should fully characterize all patients in our clinical practice and not just state that they have asthma, COPD, or asthma and COPD overlap syndrome. This detailed phenotyping can help in understanding these obstructive airway diseases and provide guidance for disease management.
University of Groningen, Department of Pulmonology, University Medical Center Groningen, Groningen, The Netherlands; University of Groningen, GRIAC Research Institute, University Medical Center Groningen, Groningen, The Netherlands. Electronic address: d.s.postma@umcg.nl.
Dirkje S
DS
Postma
Channing Division of Network Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, Mass.
Scott T
ST
Weiss
University of Groningen, Department of Pulmonology, University Medical Center Groningen, Groningen, The Netherlands; University of Groningen, GRIAC Research Institute, University Medical Center Groningen, Groningen, The Netherlands.
Maarten
M
van den Berge
University of Groningen, Department of Pulmonology, University Medical Center Groningen, Groningen, The Netherlands; University of Groningen, GRIAC Research Institute, University Medical Center Groningen, Groningen, The Netherlands.
Huib A M
HA
Kerstjens
University of Groningen, GRIAC Research Institute, University Medical Center Groningen, Groningen, The Netherlands; University of Groningen, University Medical Center Groningen, and the Department of Pediatric Pulmonology and Pediatric Allergology, Beatrix Children's Hospital, Groningen, The Netherlands.
Gerard H
GH
Koppelman
D000367:Age Factors; D001249:Asthma / Q000175:diagnosis* / Q000235:genetics / Q000276:immunology / Q000473:pathology; D016535:Bronchial Hyperreactivity / Q000175:diagnosis* / Q000235:genetics / Q000276:immunology / Q000473:pathology; D015870:Gene Expression; D059647:Gene-Environment Interaction; D005838:Genotype; D006801:Humans; D007073:Immunoglobulin E / Q000235:genetics; D020780:Matrix Metalloproteinase 9 / Q000235:genetics / Q000276:immunology; D010641:Phenotype; D020641:Polymorphism, Single Nucleotide; D029424:Pulmonary Disease, Chronic Obstructive / Q000175:diagnosis* / Q000235:genetics / Q000276:immunology / Q000473:pathology; D011656:Pulmonary Emphysema / Q000175:diagnosis* / Q000235:genetics / Q000276:immunology / Q000473:pathology; D012737:Sex Factors; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000276:immunology
C508960:TGFB1 protein, human; D053773:Transforming Growth Factor beta1; D007073:Immunoglobulin E; C579270:MMP9 protein, human; D020780:Matrix Metalloproteinase 9
Asthma; Dutch hypothesis; allergy; chronic obstructive pulmonary disease; hyperresponsiveness