Category Archives: Allergy

Allergy, Software, Vitamins

Rat race

While working on a review about vitamin D and the microbiome, I came across an interesting article Immune-Microbiota Interactions: Dysbiosis as a Global Health Issue

Recent research, however, demonstrated that a number of specific interventions can lead to (partial) primary prevention of allergy, especially of atopic dermatitis (AD) and food allergy (FA). Three types of primary prevention strategies have been successfully studied: early administration of bacterial products (most studies are on probiotics), early moisturizing in infants at risk for AD and early exposure to allergenic foods (peanut and egg).

I am not so much convinced of any successful probiotics research that prevents all kind of allergy (ref, ref, just to name two). The interesting point, however, is the new recommendation to early exposure of allergenic foods. Does earlier exposure mean less exposure under vitamin D suppression that shouldn’t start before week 6?

 

CC-BY-NC Science Surf , accessed 29.08.2026
Allergy

Window of Opportunity

I very much liked the “Window of Opportunity” in the Nestle Nutrition Workshop Series 61, published by Karger in 2008. Page 180 has an interesting account of the hygiene hypothesis:

Dr. Bier: … The other is the issue of the hygiene hypothesis, the cleaner environment. We are just in a somewhat less dirty environment, we are not in a clean environment, and that is the problem I have with that particular approach.

So, I am not alone

Dr. Barker:… I am guilty of inventing the term “hygiene hypothesis” as an explanation of the epidemic of appendicitis that followed the introduction of running hot water into housing of Western countries.

According to Sozanska et al. the hygiene hypothesis has more fathers

In 1970, Peter Preston1 posed the following question: ''Is the atopic syndrome a consequence of good hygiene?'' If this was the case, he argued that ''the manifestations of atopy . would have appeared in given areas only after standards of hygiene . had been raised to high levels.''

while David Strachan calls it a misnomer since I know him. The last occasion was in the BMJ in August 2014

As the authors correctly point out, the term “hygiene hypothesis”, which is often attributed to my BMJ 1989 paper, is actually shorthand for a line of argument established much earlier. When presenting my own work, I regularly remind my audience that the ideas presented in the BMJ 1989 paper were inspired by David Barker’s publications on acute appendicitis a year or two before. However, as the authors acknowledge, Barker’s “hygiene hypothesis for appendicitis” was in turn influenced by earlier thinking.
I also recount that the inclusion of “hygiene” in the title of my paper (along with “hay fever” and “household size”) owed more to an alliterative tendency than to my aspiration to claim a new scientific paradigm. What interested me over the subsequent years was how, after initial disdain on grounds of implausibility, the immunological community enthusiastically endorsed the concept of the “hygiene hypothesis” as soon as they had proposed a cellular mechanism to explain it!
[…]
Indeed, the frustration over 25 years of epidemiological and immunological investigation is that so little progress has been made in identifying the biologically relevant exposures which “explain” the frequently replicated epidemiological observations linking allergic sensitisation and atopic disease (inversely) to family size and to “unhygienic” environments such as farming, separately and in combination…

 

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Allergy

Allergy, Vitamin D Receptor and Parabacteriodes

There was a congress abstract earlier this year by Rachid, Rima A et al. in Journal of Allergy and Clinical Immunology: “Food Allergy in Infancy Is Associated with Dysbiosis of the Intestinal Microbiota” where 137 infants (52 food-allergic and 85 controls) were enrolled and differences in fecal microbiota tested between the 2 groups. Food-allergic babies at 1-6 months of age had decreased abundances of genera in Bacteroidetes (Parabacteroides and Alistipes).

Interestingly, a new genome-wide association study of the gut microbiota using two cohorts from Northern Germany identified genome-wide significant associations for microbial variation and individual taxa at multiple genetic loci, including the VDR gene. To further explore this association, they analyzed gut microbiota data fin Vdr-/- mice, confirming that loss of Vdr in mice substantially affects diversity. A more detailed exploration also showed that VDR consistently influences individual bacterial taxa such as Parabacteroides.

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So, is this a missing link?-Can vitamin D supplementation influence the gut microbial flora? This could explain even other observations. Right now rs7974353 is a rare human intronic SNP with no disease annotation.

 

CC-BY-NC Science Surf , accessed 29.08.2026
Allergy

Forget the hygiene hypothesis until there is a good study

A new paper in PLoS Negl Trop Dis this week reports

The hygiene hypothesis is accepted by many in the global scientific community […] However, aspects of this hypothesis are based on assumptions that may not fully account for realities about human helminth infections. Such realities include evidence of causal associations between helminth infections and asthma or inflammatory bowel disease

Talking about realities may help proponents of the hygiene hypothesis who are stuck in a never ending loop publishing observational studies.

Even the NEJM contributes to the hygiene hysteria hype this week. Although the allergic rhinitis prevalence isn’t so much lower in old order Amish (who are even a heterogenous group), the difference to Hutterite is being highlighted. I do not even understand the study design here as it is neither cross-sectional, nor case-control nor cohort study. Is it just an exposure description in two different groups? Conclusions like

sustained microbial exposure was also reflected in the phenotypes of peripheral innate immune cells in the Amish.

are strange if we believe that we humans carry more bacterial than human cells. And every smoker encounters a 120fold endotoxin concentration compared to ambient air – without getting rid of asthma or allergy.

The results of our studies in humans and mice indicate that the Amish environment provides protection against asthma

is certainly wrong – nobody knows if this is an environmental or genetic or iatrogenic factor. The key finding is IRF7 expression but unfortunately IRF7 plays a critical role in the innate immune response against viruses – and not bacteria/endotoxin…

 

CC-BY-NC Science Surf , accessed 29.08.2026
Allergy, Vitamins

Why allergy and vitamin D trials failed so far

The following figure highlights the exposure scheme in the three published vitamin D / allergy clinical trials so far: Grant 2016, Litonjua 2016 and Chawes 2016.

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None of them found anything important, maybe due to the design flaw in all these studies?

All three studies have been designed with the assumption of a beneficial vitamin D effect.

They are dose finding studies that do not allow to prove or disprove any vitamin D effect.

 

CC-BY-NC Science Surf , accessed 29.08.2026
Allergy

You get what you pay for

Finally, the Copenhagen and Boston clinical trials of vitamin D supplementation in pregnancy have been published in JAMA today. There is no protection against asthma or wheezing when comparing 4400 IU or 2800 IU vitamin D vs 400 IU vitamin D.
From basic pharmacology and immunology, this is an expected result: the only interesting point would have been to compare vitamin vs placebo. Even the editorial missed the most important point – what happens to the newborn immune system when being supplemented with vitamin D?

 

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Allergy, Software

Forget about multiple regression analysis

When starting in epidemiology I had only high school math skills. Nevertheless, I could usually find major associations by simple tables and plots. Then I learned about multiple regression analysis and used it in numerous research papers. Nevertheless I soon discovered that

The results are often somewhere between meaningless and quite damaging.

Continue reading Forget about multiple regression analysis →

 

CC-BY-NC Science Surf , accessed 29.08.2026
Allergy

Grünenthal und der Contergan Skandal

In der deutschen Wikipedia kommt die Diskussion um die gezielte Anheuerung von Nazis durch Grünenthal zu kurz, wenn man den Newsweek Artikel aus dem Jahr 2012 zu Rate zieht.
Bei diesem Artikel habe ich zum ersten Mal verstanden, warum sich die Aufklärung durch Widukind Lenz so lange hingezogen hat (ich habe von Lenz das erste Mal um 1981 in der Humangenetikvorlesung von Utermann und Wendt in Marburg gehört) – es waren alten Nazi-Seilschaften, die sich gegenseitig gedeckt haben.
Das erste Kind mit der Phokomelie wurde bereits am 25.12.1956 geboren. Dennoch brauchte es genau 5 Jahre, so k-factor, Grünenthal als Schuldigen auszumachen.

Mit Tierversuchen zu dieser Frage begannen Mückter und seine Kollegen erst im September 1961. Am 15. November 1961 erhielt Mückter dann einen Anruf des Hamburger Kinderarztes und Humangenetikers Widukind Lenz, der die Rücknahme aller Thalidomid-Produkte aus dem Handel forderte, weil seine Forschungsergebnisse einen Zusammenhang zwischen Kindesmißbildungen und Contergan nahelegten. Lenz wendete sich auch an die Behörden. Grünenthal erklärte sich daraufhin lediglich dazu bereit, auf den Packungen vor einer Einnahme während der Schwangerschaft zu warnen und drohte der nordrhein-westfälischen Gesundheitsbehörde für den Fall eines Verbotes mit einer Schadensersatzklage. Erst ein Artikel in der Zeitung “Welt am Sonntag” am 26. November (“Mißgeburt durch Tabletten?”) bewegte die Firma dazu, das Medikament am folgendem Tag aus dem Handel zu nehmen.

Der Lancet Letter vom Mc Bride am 16.12.1961 setzte dann den Schlusspunkt. Leider wurden die Restbestände aber nicht vernichtet, so dass noch Kinder bis in die Mitte der 60er Jahre mit der Behinderung geboren. Nochmal k-factor:

Die Ambivalenz ist uns erhalten geblieben, und sie findet sich wieder in den gegenwärtigen Diskussionen um Gentechnik und Embryonenforschung. Fortschritt kann Segen bringen, aber wird dies niemals ohne Nebenwirkungen tun, seien diese ökologischer oder gesundheitlicher Natur. Gegen Rückschläge des Fortschritts helfen nur vernünftige Regeln und eine kontrovers geführte Debatte.

 

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Allergy

Farm life does not prevent from asthma

In most farm children, asthma is not being prevented. And even in those children who might have had a benefit from being raised on a farm, it is not clear where the protection is mediated by: Some biological agent like endotoxin? Some healthy worker effect? Less medical interventions like antibiotics, Caesarean or vitamin D? It looks like other researchers are sceptical too

Others who study the hygiene hypothesis caution that the newly uncovered mechanism does not entirely explain the protective effect of dairy farm life. Drinking unprocessed milk also seems to ward off asthma in kids, points out Gary Huffnagle of the University of Michigan, Ann Arbor-and that effect is unlikely to involve the lung epithelium. What’s more, endotoxin levels are not that much higher on farms than in cities, suggesting "it’s too simple an answer," says asthma genetics researcher William Cookson of Imperial College London, who thinks changes in living microbial communities in the lungs and gut may be just as important.

 

CC-BY-NC Science Surf , accessed 29.08.2026
Allergy, Vitamins

A step forward in allergy research

The most recent paper of my Australian collaborators is a relevant step forward: Polymorphisms affecting vitamin D-binding protein modify the relationship between serum vitamin D (25[OH]D3) and food allergy. Basically they show an

… association between serum 25-hydroxyvitamin D3 (25[OH]D3) levels and food allergy at age 1 year (338 challenge-proven food-allergic and 269 control participants) and age 2 years (55 participants with persistent and 50 participants with resolved food allergy)… Analyses were stratified by genotype at rs7041 as a proxy marker of DBP levels… Low serum 25(OH)D3 level (<50 nM/L) at age 1 years was associated with food allergy, particularly among infants with the GG genotype (odds ratio [OR], 6.0; 95% CI, 0.9-38.9) … Maternal antenatal vitamin D supplementation was associated with less food allergy, particularly in infants with the GT/TT genotype (OR, 0.10; 95% CI, 0.03-0.41)… This increases the biological plausibility of a role for vitamin D in the development of food allergy.

Maybe it would be helpful to have also “real” DBP levels for estimating bioavailability (and even data of supplement use) but already the reported results are another strong argument for the vitamin D – allergy axis. This is also largely in line with what I predicted back in 2012

Both vitamin D insufficiency and vitamin D supplementation have been linked to allergy and asthma. This apparent paradox is explained by epigenetic programming in pregnancy by low vitamin D levels and the excessive high supplementation in the newborn period.

Maybe I should have emphasized that genetic variants in the vitamin D pathway are also important for biological effects.

 

CC-BY-NC Science Surf , accessed 29.08.2026
Allergy

Fraud, Distortion, Delusion and Consensus

Alvan Feinstein wrote a paper with this title back in 1988. Unfortunately it is not online although being a great paper. Feinstein explains that

Certain deceptions are deliberately planned frauds, but many other occur inadvertently. They arise as distortions or delusions, produced by flaws in the conventional methods used for the “standard” practice of scientific research.

We published the vitamin D hypothesis in 1999 – supplements biasing the immune system – while having in the meantime considerable empirical evidence for it.
Believe it or not, but how would you rate a review about vitamin D and allergy that reports only about BENEFICIAL effects of vitamin D? Deliberately planned fraud? Distortion? Delusion?

 

CC-BY-NC Science Surf , accessed 29.08.2026
Allergy, Genetics, Vitamins

5% of methylated sites escape reprogramming – a new allergy research direction

New Scientist Health has a short report how parents’ lives could change children’s DNA.

Azim Surani at Cambridge University and colleagues have demonstrated that some genes in the developing fetus escape the cleaning mechanism. Surani’s team analysed methylation patterns in a type of fetal cell that later forms a fetus’s own sperm or eggs. We would expect these cells to have been wiped clean when the fetus’s epigenome was reset at the early embryo stage. “However, about 2 to 5 per cent of methylation across the genome escaped this reprogramming,” says Surani.

The current wave of interest stems from three new papers: “The Transcriptome and DNA Methylome Landscapes of Human Primordial Germ Cells” by Guo demonstrates

The transcriptome of human primordial germ cells from the migrating stage to the gonadal stage reveals that both pluripotency genes and germline-specific genes are simultaneously expressed within the same individual cells. The global erasure of DNA methylation creates a super-hypomethylated germline genome.

So at week 10 after gestation, all analyzed 233 primordial germ cells lost their parental methylation marks except of 6% of the male and 8% of the female genome (which is a bit larger) . Unfortunately I did not find a list of genes there that have their parental methylation status transmitted.

Tang from a British consortium “A Unique Gene Regulatory Network Resets the Human Germline Epigenome for Development” writes

A unique transcriptome drives extensive epigenome resetting in human primordial germ cells for establishment of totipotency. Some loci associated with metabolic and neurological disorders exhibit resistance to reprogramming and are candidates for transgenerational epigenetic inheritance.

Here evolutionarily young and potentially hazardous retroelements, like SVA, remain methylated ( the number of embryos being examined is not given). Evolutionarily young and potentially hazardous retroelements, like SVA, remain methylated. When testing for resistant loci, they found that H3K9me3 marked escaping ; resistant regions were also enriched for KAP1 (alias TRIM28) binding sites of ESCs. But still no gene list there.

Sofia Gkountela “DNA Demethylation Dynamics in the Human Prenatal Germline” from the US

performed whole-genome bisulfite sequencing (WGBS) and RNA-sequencing (RNA-seq) of human prenatal germline cells from 53 to 137 days of development. We discovered that the transcriptome and methylome of human germ-line is distinct from both human PSCs and the inner cell mass (ICM) of human blastocysts … Gene expression do not correlate with global changes in DNA methylation.

In this paper finally there is the gene list, I was looking for — basically not demethylated, parentally inherited genes. Persistent methylated regions (also termed DMR, differential methylated regions) in advanced germline cells (AGCs) were seen in 500+ genes as given in table S4:

AADACL2-AS1, ABCA7, ABCC5, ABHD12, ABR, AC093375.1, ACSL4, ACSM1, ACVR1C, ACYP1, ADAMTSL3, ADARB2, ADK, AGBL4, AGK, AGPS, AIG1, AKAP9, AKR1B15, ALPK2, ANK1, ANKHD1, ANKHD1-EIF4EBP3, ANKRD11, ANKRD12, ANKRD19P, ANKRD20A9P, ANKRD24, ANKRD26, ANKRD26P1, ANKRD30BL, ANKRD31, AP2A2, AP3D1, AP4E1, ARAP2, ARHGAP26, ARHGAP39, ARHGAP44, ARHGEF18, ARHGEF4, ARHGEF7, ARID3A, ARL13B, ASB3, ASH1L, ASTN2, ASZ1, ATAD3A, ATF1, ATP11A, ATP13A1, ATP2C1, ATP8A2, ATP9B, AUH, AVEN, BAGE, BAGE2, BAGE3, BAGE4, BAGE5, BASP1P1, BAZ1A, BBS9, BCAS3, BCO2, BCYRN1, BEND3, BEND7, BRE, BRSK2, C14orf159, C15orf37, C1GALT1, C1orf159, C20orf196, C22orf34, C2orf61, C3orf67, C3orf67-AS1, C7orf50, C7orf60, C9orf3, CACNA1B, CACNG4, CALN1, CAMK1D, CARF, CARS2, CC2D2A, CCBL2, CCDC101, CCDC130, CCDC148, CCDC149, CCDC57, CCDC88C, CCDC97, CCNY, CCSER1, CD163, CD2AP, CD46, CDH12, CDH4, CDKAL1, CELF2, CEP70, CERK, CERS4, CFH, CHD2, CHD6, CHODL, CHRM5, CHRNA10, CHRNA4, CLEC16A, CLIC5, CLIC6, CNOT2, CNTN6, CNTNAP2, COG2, COL15A1, COL18A1, COL24A1, COL6A4P2, COLEC11, CORO2B, CPVL, CRTC3, CSMD1, CSMD2, CSNK1D, CTB-7E3.1, CTDP1, CTIF, CTNNA2, CTNNA3, CUBN, CXCR2, CXorf49, CXorf49B, CYCS, CYP3A5, DAPK2, DCDC2C, DDA1, DENND1A, DENND5A, DGUOK-AS1, DIP2C, DLG1, DLK1, DNAH6, DNAH8, DNAJC1, DNER, DOC2GP, DOCK1, DOCK7, DPP10, DSTN, DTNB, DYX1C1, DYX1C1-CCPG1, EBF3, ECHDC2, EDIL3, EEPD1, EFCAB10, EFCAB4B, EFTUD1, EHBP1, EIF2B3, ELMO1, EP400NL, EPHA6, EPPK1, ERC1, ERCC8, ERICH1-AS1, ERP44, ETFA, EVC2, EXD3, EXOC2, EYS, F11-AS1, FAAH, FAM172A, FAM174A, FAM207A, FAM209A, FAM86FP, FANCC, FBN3, FBXO39, FGD4, FGF14, FHIT, FIG4, FLJ30403, FNBP4, FOXN3, FREM3, FZR1, GABRA2, GAS6, GBP2, GCNT7, GDA, GGCX, GLCCI1, GLRA1, GLRA2, GMDS, GNAI1, GOLIM4, GPR75-ASB3, GRIK2, GRM7, GTF3C6, GTPBP10, GUSBP1, H6PD, HCCAT3, HCN4, HDAC4, HECTD4, HEG1, HPGD, HRNR, HS6ST3, HTR7, IFNAR1, IGF2BP3, IGSF11, IGSF22, IGSF9B, IL1RAPL2, IL31RA, IMMP2L, IMPG2, INF2, INTS1, INVS, IPO7, IQCF3, IQCG, IRAK1BP1, ISOC2, ISPD, ITFG1, ITGB1BP2, ITGBL1, JAM3, JAZF1, JMJD1C, KALRN, KATNBL1, KDM3B, KDM4C, KIAA0825, KIAA1328, KIF4A, KIF5B, KLHL20, KLHL3, LANCL3, LDB2, LDLRAD3, LHCGR, LINC00239, LINC00408, LINC00469, LINC00670, LINC00871, LINC00922, LINC01193, LINC01194, LINGO2, LMF1, LOC100128505, LOC100133669, LOC100188947, LOC100289333, LOC101927069, LOC101927280, LOC101927286, LOC101929064, LOC101929387, LOC102723742, LOC145837, LOC283683, LOC285768, LOC286083, LOC442132, LPA, LPPR1, LRP1B, LRRC4C, LTBP1, LUZP2, MAD1L1, MAGT1, MAML3, MAOA, MAP3K15, MAP4K5, MAPK10, MAPK8, MAPK8IP3, MAST2, MCTP1, MCU, MEF2A, MEI4, MELK, METTL15, METTL9, MFHAS1, MIR1273H, MIR518B, MIR518F, MIR520B, MIR548H2, MIR548O2, MIR6130, MIR6744, MOB3B, MOCOS, MTG1, MTMR7, MUC2, MUC5B, MUM1L1, MYO10, MYO5A, MYO9A, MYT1, MYT1L, NAA20, NAALADL2, NAT1, NAV2, NBPF10, NBPF20, NCALD, NCOA2, NEBL, NFATC3, NIFK-AS1, NIPA1, NKAIN2, NKAIN3, NLRP4, NME7, NOC4L, NONO, NPHP4, NQO2, NRXN3, NSUN6, NTSR1, NUBPL, NXN, OGG1, OR8S1, OSBP2, OSBPL6, OSMR, PACS2, PARK2, PARL, PAWR, PCBP3, PCDH19, PCDH9, PCNT, PCNXL2, PCSK6, PDAP1, PDE11A, PDE4D, PGAM1P5, PGAM5, PHKB, PHRF1, PIK3C2A, PIK3CA, PIP5K1B, PKD2L1, PKHD1, PKIB, PLCD1, PLCH1, PLEC, PLOD2, POLR1A, POMK, PPARA, PPARGC1B, PPP2R5C, PRH1, PRH1-PRR4, PRICKLE1, PRKAR1B, PRKCZ, PROSER2, PROSER2-AS1, PRR26, PRUNE2, PTCD3, PTDSS2, PTGFRN, PTPN21, PTPRD, PTPRN2, PYGB, RAB28, RAB3D, RAB3GAP2, RAB3IP, RABGAP1L, RAPGEF6, RBFOX1, RC3H2, RFX7, RGS6, RGS7, RNF115, RNH1, RNU6-52P, RNU6-81P, RPH3AL, RPIA, RPL35A, RPS6KC1, RSPH1, RYR1, S100Z, SCAPER, SCCPDH, SCEL, SCFD2, SCHLAP1, SCMH1, SDHAP3, SDK1, SEC14L1, SEC24D, SEL1L, SEMA3C, SERPINB3, SESN2, SESTD1, SETD1A, SETDB1, SHANK2, SHC2, SIL1, SIN3B, SLC12A3, SLC22A15, SLC24A2, SLC38A10, SLC44A5, SLC6A1, SLC8A1-AS1, SNORD115-1, SNORD115-2, SNTB2, SNTG2, SNX29, SORCS2, SOX5, SPATA5, SPIDR, SPIRE1, SPTB, SPTBN2, SPTLC3, SRD5A1, SRRM4, ST20, ST20-MTHFS, ST6GAL1, STARD9, STIM1, STK31, STK38, STON1-GTF2A1L, STXBP5-AS1, SUPT3H, SYN3, TAF1L, TAS2R19, TENM2, TENM3, THRB, THSD7B, TIMM23B, TJP2, TLK1, TMCC1, TMED1, TMEM132D, TMEM218, TMEM66, TMTC2, TNRC6B, TPST1, TPTE, TRAPPC9, TRIO, TRPC4AP, TRPM2, TRRAP, TSNARE1, TSPAN15, TSPEAR, TSSC1, TTC28, TTC40, TULP4, TYRO3P, TYSND1, TYW1B, UGGT2, UHRF1, ULK4, UNC5D, UNC79, UNC93A, USP13, USP15, USP34, USP50, VGLL4, VPRBP, VPS53, WDPCP, WDR1, WDR19, WDR36, WDR60, WWOX, XAF1, ZBTB20, ZCWPW2, ZFPM2, ZFYVE9, ZKSCAN5, ZMAT1, ZMYM4, ZNF135, ZNF14, ZNF317, ZNF32, ZNF32-AS1, ZNF32-AS2, ZNF32-AS3, ZNF335, ZNF341, ZNF350, ZNF382, ZNF415, ZNF556, ZNF595, ZNF664-FAM101A, ZNF670, ZNF670-ZNF695, ZNF7, ZNF717, ZNF718, ZNF767P, ZNF808, ZNF845, ZNRF1, ZSWIM5

(I dropped two genes as they are only date-formatted numbers in the supplied Excel sheet).

The interesting question for me is if there is an interaction with genes identified earlier in asthma and allergy research. According to the GWAS catalog there are 190 associated genes that match only 9 on the list above: AS1, CLEC16A, CTNNA3, EDIL3, PDE4D, PGAM1P5, SDK1, WDR36. Nothing exciting, in particular no HLA association. WDR36 is the only gene, we published some years ago. I find also only one match (COL15A1) of the 73 low methylation IgE loci published earlier.

Possibly, any of these persistent methylated genes can even stand on its own feet with just one silenced / activated gene being responsible for the pathology in a pedigree. I cannot identify so many signals in the list above, maybe some IL1 related stuff (IL1RAPL2, IL31RA, IRAK1BP1). CD46 at least is a good candidate as it is known that enhanced CD46-induced regulatory T cells will suppress allergic inflammation after allergen specific immunotherapy.

Unexpectedly, there are also no vitamin D related genes, no VDR, no cytochrome P450 enzymes. Nevertheless I recognize a whole bunch of calcium related genes: STIM1 (transmembrane protein that mediates Ca2+ influx), ATP11A + ATP2C1 (ATP dependent Ca2+ transporter), TRPM2 ( another Ca2+ channel), TRPC4AP + RYR1 (sarcoplasmic reticulum calcium channels) and NCALD (a cytosolic calcium transporter).

So would be definitely interesting to test the methylation status of these genes along with vitamin D levels in allergic parents and their kids.

 

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Allergy

Is this a retraction of the hygiene hypothesis?

There are news about the hygiene hypothesis.

Home cleanliness resulted only in quantitative reduction of floor dust, which mainly indicates removal of superficial dirt with a rather cosmetic effect. Conventional cleaning does not eradicate microorganisms sustainably, because emptied microbial niches are instantly recolonized by ventilation and living carrier.

Sure. Continue reading Is this a retraction of the hygiene hypothesis? →

 

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Allergy, Vitamins

U shape is good and bad

I did not expect that serum vitamin D levels are associated with mortality at both ends of the distribution as now shown by Dorup et al.

Out of 247,574 a total of 16.645 subjects died in the ensuing 0 -7 years. … 25-hydroxyvitamin D level of 70 nmol/L was associated with the lowest cardiovascular disease mortality risk … At the higher extreme (125 nmol/L), the hazard ratio of cardiovascular disease mortality was 1.3 (95% CI 1.2-1.4), with similar risk among men and women.

Following our first paper on U shaped vitamin D effects there are now many more papers show that effect. Vitamin D is not just good or bad, it is both depending on timing, dose, application, whatever.

 

U

 

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