Wheats and gluten

Sometimes it takes some personal connection to get me motivated enough to try and understand something a little more fully. Laziness, I guess. Anyway, for example, I vaguely knew about the gluten seed storage proteins of wheat and the coeliac disease they cause in about 1% of the population. But I decided to delve a little deeper only when an old friend I hadn’t seen for a while visited today and told me that she was a sufferer, and that she needed to know how to describe the condition in italian so she wouldn’t get into trouble eating in restaurants here in Rome.

Having sorted that out, I was interested to know whether there are differences among wheat species in the “toxicity” of their glutens. You’ll remember that wheat comes in a polyploid series: diploid, tetraploids and hexaploids. And that three distinct genomes are involved: AA, BB and DD. Diploid einkorn (AA) and BB genome species got together to form tetraploid emmer and durum wheat (AABB). And these hybridized with wild diploid Triticum tauschii to make hexaploid (AABBDD) bread wheat.

It turns out that differences in gluten toxicity do exist. An analysis of the ancestral A, B and D genomes of wheat found that DNA sequences associated with 4 peptides that have been identified as triggering a response in coeliac patients are not distributed at random. For example, the B genome sequences analyzed did not reveal any of the “guilty” sequences.

On the basis of such insight, breeding strategies can be designed to generate less toxic varieties of wheat which may be tolerated by at least part of the [coelic disease] patient population.

Oh, and coeliac disease is called celiachia in italian.

Food composition

The new issue of the Journal of Food Composition and Analysis has reviews of food composition activities in both Latin America and Oceania. I only have access to the abstracts, but I know that in the Pacific a lot of attention is being paid to differences in nutrient composition among varieties of crops like banana, pandanus and giant swamp taro. This is something that might be of interest to the authors of a third paper in the same issue of the journal. They look at differences in micronutrient composition within different cereal species in Mali but fail to mention this varietal dimension. They ascribe the differences to climate and ecology — at least in the abstract. Important, of course, but surely not the whole story. I’m going to try to get hold of the paper.

LATER: So it looks like what they did is collect various different samples of fonio, say, in each of several distinct eco-geographic zones and pool the samples collected in each zone for analysis. Nothing in the paper about trying to collect material with similar varietal names or anything like that. So any differences due to environment will be confounded with genetic variation. Seems to me like an opportunity missed, at best.

More on iron

As coincidence would have it, just a few days after Jeremy blogged about iron deficiency and what could be done about it, Dienekes’ Anthropology Blog flagged a paper on the diversity that exists among human populations in their predisposition to this problem. More specifically, the paper is about hemochromatosis ((Christopher Naugler. Hemochromatosis: A Neolithic adaptation to cereal grain diets. Medical hypotheses. 2007/08/10.)), an hereditary disorder that causes body tissues like the liver to absorb and store more iron than “normal.”

The hypothesis advanced by the author is that the condition arose in Neolithic farming communities as an adaptation to the lower levels of iron in a cereals-based diet as the shift from more iron-rich hunter-gatherer diets accelerated. Highlighting the complexity of nutritional issues, however, is the fact that prevalence of the guilty allele is lower in the Mediterranean and Near Eastern than in northern European agrarian regions, possibly because of the higher dietary intake of vitamin C down south — vitamin C assists in iron uptake. Such interactions are one reason why nutritional silver bullets are unlikely to exist.

Rusty conclusions about iron deficiency

Iron deficiency anaemia is a big problem. WHO estimates that about 2 billion people — that’s roughly one in three — lack enough iron in the diet. And the consequences are grave for health and the economies of developing countries. So of course people are focused on ways to combat iron deficiency. Two hog the limelight: supplementation by adding iron to the diet and biofortification, breeding to add more iron to the staples that make up the diet. A recent paper in The Lancet reviews the story of iron deficiency and how to treat it. ((Michael B Zimmermann and Richard F Hurrell, Nutritional iron deficiency, The Lancet, 370 (9586), 11 August 2007-17 August 2007, Pp 511-520.)) Perhaps not surprisingly, the study concludes that “targeted iron supplementation, iron fortification of foods, or both, can control iron deficiency in populations”. And yet, having said that “dietary iron bioavailability is low in populations consuming monotonous plant-based diets,” the authors do not appear to have seriously considered the idea of trying to attack that monotony instead. Maybe enriching and diversifying those plant-based diets to include more dark green leafy vegetables and more pulses would be as effective, with additional benefits in other realms. But that kind of intervention isn’t nearly as glamorous, and gets little attention.

Of course, it could be that solving the problem of iron deficiency will just give rise to other difficulties. Another paper suggests that iron deficiency protects us against some of the epidemic contagious diseases that have hitched along as people crowded together in agriculturally-fed cities. ((S Denic and M Agarwal, Nutritional iron deficiency: an evolutionary perspective. Nutrition. 2007, 23:603-14. Epub 2007 Jun 20.)) Maybe iron deficiency — at least in moderation — is a good thing?