Learning Objective
Özkan, H., Brandolini, A., Schäfer-Pregl, R., & Salamini, F. (2005). AFLP analysis of a collection of tetraploid wheat indicates the origin of emmer and hard wheat domestication in southeast Turkey. Molecular Biology and Evolution, 22(10), 1997-2007. This study discusses the genetic diversity of einkorn wheat and provides information on the origin of wheat domestication. It also mentions that einkorn has a simpler genetic makeup compared to modern wheat varieties.
Estimated time: 15 mins.
2016 – iPhone video – 900m above sea level, meeting the farmers who grow the einkorn we use.
Einkorn (Triticum monococcum) is diploid — it has a completely different gliadin gene repertoire to modern bread wheat. When researchers have mapped the known coeliac epitopes, those specific gluten peptides that, once deamidated by tissue transglutaminase, bind to HLA-DQ2 or DQ8 and activate pathogenic T cells, they’ve found that certain einkorn genotypes carry fewer of these canonical toxic sequences. Some carry variants that are simply less stimulatory.
The gliadin proteins in wheat are responsible for triggering an immune response in people with coeliac disease or gluten sensitivity. The 33-mer gliadin peptide, found in alpha-gliadin, is particularly immunotoxic — it triggers the strongest immune response. Einkorn lacks this highly immunotoxic 33-mer gliadin peptide found in modern wheat varieties.
One of the reasons modern wheat is so problematic is that certain proline- and glutamine-rich peptides resist our human proteases. They persist long enough to trigger an immune response. But when you look at in vitro digestion work comparing ancient and modern wheats, you see higher digestibility of einkorn gliadin fractions and, in parallel, reduced immune-stimulatory activity on intestinal T cells from people with coeliac disease. The mechanism is straightforward: if fewer long, intact peptides survive gastric and pancreatic digestion, there’s less antigenic substrate available for tTG deamidation and HLA presentation. This is cultivar dependent — not all einkorn behaves the same way — but it’s a real finding.
What I find particularly interesting is the role of amylase-trypsin inhibitors, the ATIs. Coeliac immunopathology isn’t only adaptive — innate activation and epithelial stress can amplify the whole response. ATIs are non-gluten wheat proteins that trigger innate immune signalling, and they’re implicated in wheat-related inflammatory responses beyond coeliac disease itself. Several comparative studies show that ATIs from einkorn have reduced potential to elicit innate immune
responses compared to modern bread wheat. If that innate priming is lower, downstream inflammatory amplification may be dampened, even when gluten is present.
There’s also the architecture of the gluten itself to consider. Einkorn’s gluten network behaves differently because its storage-protein composition and polymeric structure are different. This shifts the entire “peptide landscape” the gut encounters — something explored in detail in the research on gliadin, zonulin and gut permeability.
And then we come to what happens when you combine genetics with proper processing. This is where it gets really exciting for us as bakers. Long fermentation — particularly sourdough — combined with subsequent gastrointestinal digestion can markedly reduce the size and reactivity of gluten polypeptides. The proteolysis achieved by sourdough lactic acid bacteria degrades multiple einkorn peptides, including known T-cell epitopes. Research confirms that sourdough fermented breads are more digestible than those made with baker’s yeast alone. The combination of einkorn’s protein properties plus proper fermentation pushes the peptide pool further away from the highly immunogenic forms that drive coeliac pathology.
The Research: Protective Effects of ID331 Triticum monococcum Gliadin
Study: Protective effects of ID331 Triticum monococcum gliadin on in vitro models of the intestinal epithelium Authors:Roberta Lupi, et al. Journal: Food Chemistry Year: 2016
This study explored the response of intestinal cells to einkorn gliadin compared to modern wheat gliadin. The findings are genuinely significant:
ID331 gliadin proteins from Triticum monococcum do not cause the same cell toxicity effects as gliadin from modern wheat (Triticum aestivum). This protective effect comes from ID331 ?-gliadin and its gastrointestinal-resistant peptide ?(105-123). The specific sequence of ID331 ?-gliadin is not present in all T. monococcum genotypes, which means there are variations among different einkorn varieties — cultivar selection matters.
The researchers suggest that T. monococcum might have a protective effect on the small intestine of people with coeliac disease. A diet based on T. monococcum could potentially delay or prevent the development of coeliac disease in individuals who are at risk, such as those with first-degree relatives who have the condition.
Important: This is a mechanism for reduced provocation, not permission. Einkorn still contains gluten, and the current clinical standard of care for diagnosed coeliac disease remains a strict gluten-free diet. But for those who struggle with modern wheat without having coeliac disease, and for understanding why heritage grains processed properly might be experienced differently in the body, this research matters profoundly.
Further Reading
- Nutritional properties of einkorn wheat (Triticum monococcum L.)
- Professor Michael Gänzle – Digestibility & Non-Celiac Gluten Sensitivity Lecture
- Bake with Einkorn Flour
Learning Outcome
It is essential for individuals with gluten sensitivity or intolerance to consult a healthcare professional before introducing einkorn into their diet, as individual responses may vary.
