A fantastic opening ceremony in Istanbul at the EAACI congress   Leave a comment

We have had an exceptional evening at the 30th EAACI congress, opening ceremony. We have handed out the once in a lifetime award for contributions in immunotherapy to Bill Frankland, to celebrate the 100 years of immunotherapy after the Noon paper in the Lancet. We have had a great opening ceremony in the emotional heart of Turkish society. And we had a welcome reception outdoors without being exposed to the rain the metereologists were talking about…

Thank you Ömer, and Turkey, and all friends of EAACI

Jan Lötvall

Current President of EAACI

Posted June 11, 2011 by Jan Lötvall in Uncategorized

Welcome to Istanbul, and 100 years of immunotherapy, a price to a 99 year old allergist   Leave a comment

It is with huge pleasure that I can welcome all readers to the 30th EAACI congress in Istanbul, and the opening ceremony today on the 11th June 2011. Today it is 100 years + one day since Leonard Noon published his historic paper on Immunotherapy “PROPHYLACTIC INOCULATION AGAINST HAY FEVER” in the Lancet. EAACI is celebrating this in many ways, one being the handing over of the “once only” Leonard Noon award, to the investigator that first published a controlled trial in immunotherapy, William Frankland. Bill was also a Secretary General and a President of EAACI, around 50 years ago, and still energetic and ambitious on his 99th year. The 2011 EAACI congress promises to be a fantastic event, with the best scientific programme possible, in the exciting surrounding of Istanbul. Thank you to Ömer Kalayci, the Congress President, as well as Lars Paulsen and Christian Virchow, who have coordinated the Scientific programme committee to produce this excellent programme. And also huge thanks to Cezmi Akdis, the current vice President of Congresses, Susanne Rothschild, the congress manager of EAACI, as well as the Congrex team, that have all contributed to create this exceptional event. I look forward to seeing you in Istanbul in the next few days.

Jan Lötvall

EAACI President for another two days.

Posted June 11, 2011 by Jan Lötvall in Allergy, asthma, EAACI

Stating ”race” enforces racism? Should the US Census ask people to state “race”?   Leave a comment

Stating ”race” enforces racism? Should the US Census ask people to state “race”?

On the web site of Time magazine, US Census Bureau Director Robert Groves is interviewed http://ti.me/jxmHcq. He is reporting that a large number of US citizens state more than one race. In Europe we do not state “race” when counting the population, because it is so difficult to understand what it means. And it supports feelings such as racism.

The New York Times had a series of articles on the topic earlier in the year http://nyti.ms/hf5trL. More and more Americans do not know what to tick when they have to state “race”. Personally I think the term “race” should be skipped, as it more describes social structures and history, rather than genetically important differences. Actually, race implies that the individuals “phenotype” is related to “geographic ancestry” http://en.wikipedia.org/wiki/Race_(classification_of_humans). The definition is certainly drifting away from the genetic definition, towards a more social explanation. However, it is also discussed that scientific studies through the twentieth century has found no biological basis for the classification of race, and perhaps a primary factor in racial classification has been the social conventions established during the colonial period. For example, what is “African American”. There is no clear definition to be found, except “at least one ancestor from sub-saharan Africa”. If we reverse that definition, it is absolutely clear that Barack Obama is IRISH (next time, plese do not tick “black or African American”! Actually, tick nothing…

I think the US Census should stop requiring citizens to state“race” because it is a term that enforces racism http://bit.ly/ilkptl. One could just as well describe “culture”, because that would better explain how society develop and how cultural interactions shape the world. Most NY-times readers seem to agree http://nyti.ms/e6tE6k.

Posted May 31, 2011 by Jan Lötvall in behaviour, psychology, race, science, US Census

Having ”suicidal ideation” is associated with being a smoking young asthmatic – a key risk factor for having severe asthma?   Leave a comment

Having ”suicidal ideation” is associated with being a smoking young asthmatic – a key risk factor for having severe asthma?

I saw an abstract today on pubmed, linking “suicidal ideation” and smoking in young adults with asthma. This study originates in Korea, and is published locally, but is certainly interesting also from a global perspective.

Suicidal ideation is “a common medical term for thoughts about suicide, which may be as detailed as a formulated plan, but without the suicidal act itself”. The Korean colleagues have gathered data from a very large cohort (>75000 individuals), and identified a large cohort of asthmatic smokers. Indeed, the data showed that smoking was more common in asthmatic youths, than in non-asthmatics, and there was a significant interactions between asthma and suicidal ideation with cigarette use behavior http://1.usa.gov/mdVkCm . The authors conclude that “particular attention should be paid to the awareness of health risks of cigarette smoking and mental health problems among asthmatic adolescents”.

These data certainly support the research line in our research centre, looking at personality traits in relation to adherence to asthma medication http://bit.ly/lxQIOr and http://bit.ly/fZu7WL. Personality, psychology, psychopathology, health behavior and adherence to medication are certainly key factors in some patients with severe asthma. An interesting older paper from the Leiden group with Elisabeth Bel and colleagues http://bit.ly/jYnQr1

Posted May 28, 2011 by Jan Lötvall in Uncategorized

New England Journal of Medicine paper on asthma, suggesting that remodeling is a result of airway narrowing, not the other way around…   Leave a comment

New England Journal of Medicine paper on asthma, suggesting that remodeling is a result of airway narrowing, not the other way around…

It is generally suggested that airway wall remodeling in asthma is a result of active inflammatory processes. In the current study in the prestigious New England Journal of Medicine http://bit.ly/kLYWwT , investigators from Southampton suggest that induction of bronchoconstriction by itself can induce some signs of remodeling, without a parallel process of enhanced inflammation occurring. What the investigators did, was to induced airflow obstruction by provocation with allergen, which induces significant eosinophilic inflammation, or with methacholine, which does not induce inflammation. Control groups were given either a bronchodilator or the vechicle for the provocation (saline). Importantly, the challenges were given repeatedly, which is not normally done in clinical research. Different profiles of lung function changes were observed after the challenges, with a late response being induced by allergen, and no late response observed after methacholine.

The key finding reported is that both allergen- and methacholine provocation increased subepithelial collagen-band thickness, to a similar degree. However, the measured changes were really small in both instances, but the photomicrographs shown are impressive. The statistics was based on µg change in “collagen-band” thickness, and on average the change was reported to be around 2µm for each of the challenges. Baseline thickness in asthma has been reported to be around 10µm, but variable between patients. In the current paper, it was reported to be on average 7.47-10.76 in the different groups. Thus, any observed change was in the region of 20%.

The authors conclude that “Bronchoconstriction without additional inflammation induces airway remodeling in patients with asthma. These findings have potential implications for management.” Subepithelial fibrosis has indeed been suggested to be one sign of remodeling in asthma, but its role to induce airway narrowing has been questioned. Furthermore, perhaps other challenges, such as dry air isocapnic hyperventilation or exercise should be tested, to determine whether any bronchoconstricting event can have such results.

I was disappointed that no “primary variable” was reported in the paper. Further, the statistics were allowed to be “one way”, which is unusual in medical research. New England Journal of Medicine usually is tough on those issues…

In summary, yes, the usual. More research is required to confirm these findings…

Posted May 28, 2011 by Jan Lötvall in Uncategorized

What is severe asthma, a separate disease or a mixture of diseases? And how should it be defined?   2 comments

What is severe asthma, a separate disease or a mixture of diseases? And how should it be defined?

Bel and colleagues recently published a review on the “diagnosis and definition of severe asthma”, as a consensus from the Innovative Medicine Initiative/ in Thorax: http://bit.ly/knWXTZ . Also recently, Bousquet and collagues defined different types of “severe asthma”, as “uncontrolled asthma which can result in risk of frequent severe exacerbations (or death) and/or adverse reactions to medications and/or chronic morbidity (including impaired lung function or reduced lung growth in children)” / The publication in Journal of Allergy and Clinical Immunology: http://bit.ly/iDFBxG.
They continue by dividing severe asthma into three separate subgroups including

1) untreated severe asthma,
2) difficult-to-treat severe asthma,
3) treatment-resistant severe asthma (for which asthma control is not achievable with intense therapy).

Do these publications help the scientific community in understanding “severe asthma”. In a way, they are helpful to improve the nomenclature, but obviously they are using different wordings (for example “treatment resistant” vs “refractory” – which may be similar but not exactly the same). And are they based on scientific data? The answer to that is – yes and no…

Firstly, we do not have a common definition of severe asthma, although clinicians around the world understand that they have a group of patients that are really difficult to manage, because their asthma just does not get better. In fact, there are multiple reasons for that happening. Firstly (and perhaps most commonly), patients with asthma are very often not taking their medication as prescribed: http://bit.ly/iZUv88 and http://1.usa.gov/lv1i4N. Secondly, there is a subgroup of patients which simply have a severe intrinsic disease, that is difficult to control with normal medication, as proposed by Bel and colleagues http://bit.ly/knWXTZ . Thirdly, a large group of individuals with severe asthma have so called “co-morbid diseases”, which includes obesity, severe rhinitis and chronic rhinosinusitis http://bit.ly/jqrFke and http://bit.ly/kzIuLd . We have recently shown that a series of different risk-factors exist for severe asthma in a population-based sample.

The West Sweden Asthma Study sent out 30000 questionnaires to a random population in the region, had a 62% response rate, and identified a prevalence of asthma of 8.5% in this stable and normally distributed population. Further, the prevalence of SEVERE ASTHMA, as defined by individuals having multiple daytime symptoms, was found to be approximately 2%: http://respiratory-research.com/content/10/1/94. The risk factors of having this definition of “severe asthma” was:

1) Symptoms of rhinitis
2) Signs of Chronic rhinosinusitis
3) Female sex
4) Exposures to dust and fumes
5) Obesity (BMI>30)
6) Heredity of asthma and allergy.

Thus, co-morbidites (point 1, 2 and 4) were clear risk factors. Hereditary components, presumably related to intense intrinsic disease, were only related to two of the risk factors (points 3 and 6). Otherwise, exposures are also obvious important (point 4). Details are found here: http://bit.ly/jBgoyX and http://bit.ly/dEvEsh .
Thus, this definition of severe asthma (multi symptom asthma) identified THREE individual causes of severe asthma

1) Comorbidities (Severe rhinitis, Chronic rhinosinusitis and Obesity)
2) Herediatary components (family history and/or female sex)
3) External exposures.

Is severe asthma one disease? The answer is without question NO. It is not. We have to look at the facts, and follow the evidence, to really fully understand whatever we wish to call “severe asthma”. We should follow the advice of Bertrand Russel as referenced in my blog posting from earlier today: http://bit.ly/jt0Fvi

Posted May 28, 2011 by Jan Lötvall in Uncategorized

The core of science and politics, wise words by Bertrand Russel   Leave a comment

There is a lot of politics in science, and arguing about this that and the other. We scientists see it all the time, and perhaps we sometimes forget the core of science: Finding the Truth. And only the Truth… And when we find the truth, there is not much to argue about… As long as we agree with it…

And in politics, there is one core principle that is important. Live in peace!

These two core principles of humanity were well described by Bertrand Russel in this old interview, when asked “what advice would you like to give to future generations”:

Thank you Maneck for directing me to this video.

In the exosome field we are searching for consensus to be able to establish the truth. By using crowdsourcing. Are we trying to bridge science and politics, to avoid conflict. Maybe. And to find the truth and provide opportunities to communicate that truth.
From my previous blogpostings: