Category Archives: Allergy

Does Acinetobacter lwoffii F78 protect from allergy?

When reading a new Science immunology paper (“Inception of early-life allergen-induced airway hyperresponsiveness is reliant on IL-13+CD4+T cells“) one could again think that A. lwoffii could protect from the development of house mite allergy.

The paper, however, leaves it open (even doesn’t mention the result in the discussion) if this is any specific A. lwofii effect or just some some LPS  effect that antagonized the vitamin D containing food.

So no news even 10 years  after the initial Acinetobacter hype. The only verified fact remain several deaths caused by Acinetobacter in newborns.

Finding the allergy cause

Genomics did not really help to explain allergic mechanisms beyond IL33. But combining  now stem cell & immune cell Identity tracking looks like a promising strategy for identifying initial disease events. At least colleagues at the MDC  think so.

LifeTime – ein visionärer Vorschlag für ein EU-Flagschiff. Zuverlässig vorherzusagen, wann eine Krankheit ausbricht oder wie sie verläuft, erscheint wie ein Traum. Ein europäisches Konsortium will ihn Wirklichkeit werden lassen und dabei vor allem neue Technologien der Einzelzellbiologie nutzen. Führende Forscherinnen und Forscher haben daher einen Antrag für ein FET-Flagschiff mit dem Namen LifeTime eingereicht.

Unspezifische Impfeffekte als Allergieprävention?

Unspezifische Impfeffekte  wird es wohl  geben, so der neue SPON Artikel von heute

Allerdings wird in Industrienationen daran geforscht, wie die unspezifischen Effekte früher Impfungen möglicherweise ein Leben nachwirken. Zurzeit läuft zum Beispiel eine große Studie in Australien zur Frage, ob eine frühe BCG-Impfung (gegen Tuberkulose) das Allergierisiko senkt.
Vielleicht hängt der Anstieg von Allergien ja damit zusammen, dass wir aufgehört haben, gegen Pocken und BCG zu impfen”, vermutet Aaby. Er fragt sich sogar, ob das Einstellen der Pocken-Impfung nicht auch Schaden angerichtet haben könnte, weil nun das Immuntraining durch diese Impfung ausfalle.

Der Bezug zu den Allergien ist allerdings sehr unwahrscheinlich, siehe Arnoldusson

We identified 767 articles, of which 17 satisfied our inclusion criteria; there was only 1 randomized controlled trial, with the remaining studies being epidemiologic investigations. Meta-analyses did not show any protective effect of vaccination against the risk of sensitization, as judged by specific IgE tests or skin prick testing …BCG vaccination is unlikely to be associated with protection against the risk of allergic sensitization and disease.

Es ist mir also ziemlich schleierhaft, warum das Murdoch Childrens Research Institute dazu eine Studie macht. Aber das Research Institute hat schon ganz andere Flops produziert…

Auch die Pockenimpfung schützt nicht, das ist eigentlich längst abgehakt

We found no association between having been vaccinated against smallpox in childhood and risk of atopy or allergic rhinitis. Smallpox vaccination was associated with a slightly decreased risk of asthma. There was no association between age at smallpox vaccination and risk of atopy, allergic rhinitis, or asthma. Adjusting for birth cohort, sibship size, age of the woman’s mother at birth, and social class in childhood did not change these results.

Es geht hier auch nicht so sehr um eine neue wissenschaftliche Diskussion, sondern um die journalistische Aufarbeitung eines “Dokumentarfilms”.

Nach  Masernimpfung hat im übrigen Seif Shaheen in Guinea-Bissau mehr(!) Allergien gefunden, was aber wohl auch fraglich ist, da hier nicht nur die Impfung, sondern die medizinische Betreuung generell (“iatrogen”) zur Debatte steht. Interessanterweise wird in Guinea-Bissau auch Vitamin D zur Tbc Prophylaxe gegeben wobei Vitamin D selbst ein Allergierisikofaktor ist.

Gene methylation in newborns is changed by maternal vitamin D supplementation

A randomized controlled study of pregnant women examined 400 IU vitamin D3 vs 3,800 IU from the second trimester through 4-6 weeks postpartum by genome-wide DNA methylation in leukocytes.

At birth, intervention group mothers showed DNA methylation gain and loss at 76 and 89 cytosine- guanine (CpG) dinucleotides, respectively, compared to controls. Postpartum, methylation gain was noted at 200 and loss at 102 CpGs. Associated gene clusters showed strongest biologic relevance for cell migration/ motility and cellular membrane function at birth and cadherin signaling and immune function at postpartum.

It seems that D3 supplementation is generating epigenetic effects in the offspring, something that we predicted already in 2012 as programming of vitamin D sensitivity.

When re-annotating the genes above using biocLite(“mygene”) there are at least 2 interesting genes for gain of methylation are getting to the surface: ZMIZ1  T cell differentiation) and CYP7B1 (first reaction in the cholesterol catabolic pathway of extrahepatic tissues, which converts cholesterol to bile acids). But also methylation loss is interesting with HLA-A (antigen processing).

Framing

As a particular view, framing comprises a set of concepts and theoretical perspectives on how individuals, groups, and societies, organize, perceive, and communicate about reality. I believe it is not an inherent aspect of social sciences but of science in general. Take for an example allergy research: Framing in 1980 was air pollution, in 2000 it was hygiene and in 2018 it is omics while basic research is being largely ignored. So we could rewrite the framing article

Framing involves construction of a scientific reality– by pubmed, congresses, mass media, funding agencies, prize winners, or other scientists and organizations. Participation in a language community necessarily influences an individual scientists’s perception of the meanings attributed to words or phrases. Politically, the language communities of science, advertising, religion, and mass media are highly contested and evolve imperceptibly and organically over cultural time frames.

Esoteric science

“Planetary science” – just esoteric blahblah? Embracing the whole world? Exposome instead of enviromental exposure? The desperate reaction to many unresolved questions?

The importance of the exposome and allostatic load in the planetary health paradigm.
Logan AC, Prescott SL, Haahtela T, Katz DL.
In 1980, Jonas Salk encouraged professionals in anthropology and related disciplines to consider the interconnections between “planetary health,” sociocultural changes associated with technological advances, and the biology of human health. The concept of planetary health emphasizes that human health is intricately connected to the health of natural systems within the Earth’s biosphere; experts in physiological anthropology have illuminated some of the mechanisms by which experiences in natural environments (or the built environment) can promote or detract from health. For example, shinrin-yoku and related research (which first emerged from Japan in the 1990s) helped set in motion international studies that have since examined physiological responses to time spent in natural and/or urban environments. However, in order to advance such findings into planetary health discourse, it will be necessary to further understand how these biological responses (inflammation and the collective of allostatic load) are connected to psychological constructs such as nature relatedness, and pro-social/environmental attitudes and behaviors. The exposome refers to total environmental exposures-detrimental and beneficial-that can help predict biological responses of the organism to environment over time. Advances in “omics” techniques-metagenomics, proteomics, metabolomics-and systems biology are allowing researchers to gain unprecedented insight into the physiological ramifications of human behavior. Objective markers of stress physiology and microbiome research may help illuminate the personal, public, and planetary health consequences of “extinction of experience.” At the same time, planetary health as an emerging multidisciplinary concept will be strengthened by input from the perspectives of physiological anthropology.

How does vitamin D imprinting work?

I have  predicted an epigenetic regulation of vitamin D converting enzymes in 2010 to explain the programming effect of vitamin D supplements on later allergy.
Last week, a first study examining vitamin D supplement effects in newborns has been published. They compare 400IU versus 3800IU while I am already convinced that 400 IU has some measureable effect.

 

table 2 screenshot of selected rows

 

So maybe I was wrong with my prediction of a differential CYP24A1 methylation, as the authors now describe CYP7B1. CYP7B1 encodes for 25-hydroxycholesterol 7-alpha-hydroxylase which is more upstream in the  synthesis of cholesterol.

Cure asthma: Pseudoscience?

I just came around of an EU funded research program “Cure, Eubiosus Reinstatement Therapy” that has many characteristics of quack science.

For a definition of quackery I suggest to look for Continue reading Cure asthma: Pseudoscience?

Where have all the flowers gone?

Congress: European Academy of Allergy and Clinical Immunology
Congress: 2018 Munich
Session number: OAS 03
Session title: Pan-omics in respiratory and skin disorders
Session date: Sunday, 27 May 2018
Session time: 10:30 – 12:00
Session room: Hall C
Abstract number: 0012

Continue reading Where have all the flowers gone?

Refutation of the vitamin D hypothesis?

A new epidemiological study arguments against vitamin D inducing later allergy (Parr et al., Vitamin A and D intake in pregnancy, infant supplementation, and asthma development: the Norwegian Mother and Child Cohort, Am J Clin Nutr 2018;107:789-798). Table 5 in the most recent paper shows no effect when correlating first year of life supplementation and later asthma.

 

But why did they authors not even cite our study from 2004 (Hyppönen et al. Infant Vitamin D Supplementation and Allergic Conditions in Adulthood Northern Finland Birth Cohort 1966.  Ann. N.Y. Acad. Sci. 1037: 84-95) ??

 

Although our interest was more with allergy there have been clear effects on asthma  that have been confirmed now two dozen times.  Why did the authors miss that effect?

  • The cohort consists of 115,000 children but only 55,000 are analyzed. So selection bias is omnipresent.
  • A key issue is the definition of “asthma” as “having ≥2 pharmacy dispensations of asthma medication within a 12-month interval, which is more a “last resort” option than a correct diagnosis. “We cannot rule out some misclassication in our asthma outcome“. I agree.
  • Another issue is the unrecorded vitamin supply by standard baby food in the range of 500-1000 IU/daily. Does it make any sense to test for excess supplements in a population that is already heavily exposed to >90%? “A limitation of this study is that we did not have data on nutrient intake from supplements in infant“. I agree, it makes the study worthless.
  •  The supplementation with cod liver oil, vitamin D and multivitamins is chaotic as been shown in the last row of table 5. In real life or just in this paper? Numbers are contradicting “Vitamin D only, sometimes” and “daily” do not add to the number given for “vitamin D only” in the “combined use” section.
  • Supplementation at  month 6 is even a late event if we believe that the first allergen contact under vitamin D exposure is  being important.

So, still not need to drop the vitamin D hypothesis.

Stop public funding of this sort of work

One of my most favorite blogs write

We have absolutely no reason–or, at least, no need–to criticize anything about individual mapping papers. Surely there are false findings, mis-used statistical tests, and so on, but that is part of the normal life in science, because we don’t know everything and have to make assumptions, etc. Some of the findings will be ephemeral, sample-specific, and so on. That doesn’t make them wrong. Instead, the critique should be aimed at authors who present such work with a straight face as if it is (1) important, (2) novel in any really novel way, and (3) not saying that the paper shows why, by now with so many qualitatively similar results, we should stop public funding of this sort of work. We should move on to more cogent science that reflects, but doesn’t just repeat, the discovery of genomic causal (or, at least, associational) complexity.

Maybe I see also good reasons to criticize individual mapping papers.

Loss of IL33 -/- protects against allergy

A new paper in Nat Comm shows the power of natural human gene knockouts. Maybe the finding is not really novel but it finally proves the candidate genes – the most important asthma/allergy paper in the last 2 years!

IL33, FLG, HLA-DQB1
GSDMB, BTN3A2, CCHCR1

This is even a nice addition to the most recent review of primary atopic disorders although IL33 is only depicted there in Fig 1.