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Barn TYP 1 och mammans glutenintag - nya studie

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Ny register- och frågeformulärstudie visar stark association mellan mammans glutenintag och att barnet utvecklar TYP 1 diabetes. Zoe Harcombe  publicerar snart sin kommentar.  

What is already known on this topic

 In an animal model of type 1 diabetes, a gluten free maternal diet during pregnancy almost completely prevented type 1 diabetes in offspring

 However, human studies have not shown an association between maternal gluten intake during pregnancy and the risk of type 1 diabetes in offspring

What this study adds

 In a study population of 67 565 pregnancies (63 529 women), the incidence of type 1 diabetes among children in the cohort was 0.37% (n=247) with a mean follow-up period of 15.6 years (standard deviation 1.4)

The risk of type 1 diabetes in offspring increased proportionally with maternal gluten intake during pregnancy (adjusted hazard ratio 1.31 (95% confidence interval 1.001 to 1.72) per 10 g/day increase of gluten intake)

 Mothers with the highest gluten intake versus those with the lowest gluten intake (≥20 v <7 g/day) had double the risk of type 1 diabetes development in their offspring (adjusted hazard ratio 2.00 (95% confidence interval 1.02 to 4.00))

 

https://www.bmj.com/content/362/bmj.k3547.long

https://www.webmd.com/baby/news/20180919/gluten-in-pregnancy-tied-to-babys-type-1-diabetes#1

Begränsningar i studien.

Despite the large study size, the statistical power of our study was still modest because of the low number of cases of type 1 diabetes (n=247) in our study population, which was reflected by some associations that were only just below the threshold set for formal significance (α=0.05).

In addition, the role of unmeasured or unidentified confounders can never be fully excluded in observational studies. Confirmation of our findings in another comparable but independent dataset is therefore warranted.

Dietary assessment methods that rely on the participants’ ability to report their habitual diet are inevitably subject to uncertainties, owing to the inherent difficulty in recalling diet accurately.

Although gluten containing foods are easy to identify, and the protein fractions of gluten in wheat, rye, and barley are known, gluten is also intentionally added during production to certain types of flour, bread, and other foods, which we were unable to account for.  This unaccountable addition of gluten would lead to a systematic underestimation of intake.

Another limitation was that we do not know whether mothers with a low intake of gluten during pregnancy also serve a low gluten diet to their infants. However, in our animal experiments, a gluten free diet fed to mothers during pregnancy was far more effective in preventing diabetes in the offspring than a gluten free diet fed to the offspring.

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Bli prenumerant på Zoes artiklar så kan man läsa hela.

Länk till Zoe: http://www.zoeharcombe.com/2018/09/type-1-diabetes-and-gluten/

This week’s interesting paper was genuinely attention grabbing for the simple reason that it reported an association of double. We are so used to seeing claims such as “red meat increases risk by 10%” or “whole grains reduce risk by 15%” that an association of double is of real interest. This is the starting point for the Bradford Hill criteria – if the strength of association is double, then the other eight criteria are worth looking at for potential causation and not just association (Ref 1). Bradford Hill would not consider any of the epidemiological reports of 10-20% here or there to be worth any further investigation.

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