There seems to be more evidence for the fake food hypothesis that I raised here some years ago. It says in brief that our

food recognition process is largely fooled by pre-processed food that contains additives changing appearance, taste and smelling.

while an empirical proof is still missing. But wait there is a new study about functional ankyrin-B mutations(which are believed to be a food sensing molecule although such a link is not so strong. Anykyrin-B made by the ANK2 gene is described by Vann Bennett in Science Signalling 3/113 to be associated with type II diabetes. What’s about obesity?

A new Science Perspective Paper writes about “reliable noise” which may not be the best description for a valid observation (Show me more…)

A new feature article in Nature about sparse coding let me wonder if we could construct also some Waddington-like picture of the SNPxSNP landscape as well as a disease traits and apply such an algorithm to that picture. I did some research but didn’t find any example exploiting that idea; maybe it’s even more useful with the current shift to full genomes?

We had Aulchenko here a year a go or so – now here comes his new paper Predicting human height by Victorian and genomic methods

In a population-based study of 5748 people, we find that a 54-loci genomic profile explained 4–6% of the sex- and age-adjusted height variance, and had limited ability to discriminate tall/short people, as characterized by the area under the receiver-operating characteristic curve (AUC). In a family-based study of 550 people, with both parents having height measurements, we find that the Galtonian mid-parental prediction method explained 40% of the sex- and age-adjusted height variance.

yea, yea.

What do all these places share? Spitalfriedhof Basel, Roopkund Lake, Catacombes de Paris and Central Yakuts are all examples where remains are available for genetic studies (even Tutankhamun was undergoing a paternity test recently).
More relevant will certainly be an empirical investigation if reduced selection is leading now to immune disease.

While some of my earlier co-workers continue to praise the achievements of GWAs, some other earlier co-authors now show that the common variants thrown on the current GWA chips are leading to false assocations (called politely “synthetic” associations)

We propose as an alternative explanation that variants much less common than the associated one may create “synthetic associations” by occurring, stochastically, more often in association with one of the alleles at the common site versus the other allele. Although synthetic associations are an obvious theoretical possibility, they have never been systematically explored as a possible explanation for GWAS findings. Here, we use simple computer simulations to show the conditions under which such synthetic associations will arise and how they may be recognized. We show that they are not only possible, but inevitable…

The proof comes with a sickle cell anemia study (Show me more…)