Calling BiG – does this work?

So additive to stop bread going mouldy fingered for causing diabetes.

In a small trial involving humans, people who consumed propionate experienced temporary increases in insulin resistance, over the space of a few hours, compared with those who didn’t consume the additive.

However, this early research cannot prove that propionate causes diabetes. Larger studies conducted over longer periods are needed to better understand whether propionate contributes to diabetes in people, the authors said. [9 Disgusting Things That the FDA Allows in Your Food]

Still, the findings are concerning given how widely propionate is used, the authors wrote in their paper, published today (April 24) in the journal Science Translational Medicine. They called for more research into the potential metabolic effects of food components like propionate.

“Understanding how ingredients in food affect the body’s metabolism at the molecular and cellular level could help us develop simple but effective measures to tackle the dual epidemics of obesity and diabetes,” study senior author Dr. Gökhan Hotamisligil, a professor of genetics and metabolism at the Harvard T.H. Chan School of Public Health, said in a statement.

Entirely happy with the idea that more research should be done. Just wondering whether the idea has nay legs at all is all:

Propionate is “generally recognized as safe” (GRAS) by the U.S. Food and Drug Administration (FDA), meaning the ingredient doesn’t need to be approved by the FDA to be added to food. It’s also a naturally occuring fatty acid, produced by our gut bacteria when it breaks down fiber. But no one had investigated the metabolic effects of propionate when it’s consumed as a food additive, the authors said.

If you eat fibre your gut produces it. Eating fibre has effects upon insulin etc.

So, what’s the difference here between the effect of eating fibre and eating the substance? Is there something about digestion that I’m missing here?

16 comments on “Calling BiG – does this work?

  1. Sceptical, for all sorts of reasons. Once it hits the mainstream media that scepticism will increase tenfold.

  2. Well it’s a fat so by definition will cause some degree of insulin resistance. Why would you care about whether it is eaten or is produced by bacteria? Two things come to mind. First a satiety effect – long-chain fatty acids make you feel full, short chain fatty acids don’t. Second, most fats you put in your stomach are absorbed in the small intestine. Those that get generated in the colon are probably absorbed to a lesser extent*.

    A gram a day of empty fat calories adds up to a lot over a metabolic lifetime.

    *: But I am speculating wildly and this isn’t my area.

  3. Aren’t ethnic minorities more vulnerable to this than the locals? Are they eating more or less of this bread than the locals?

  4. Rob Q1: Yes.
    Rob Q2: Who knows? Or cares? You’re not trying to do a univariate analysis on a multivariate problem there, are you 😉

  5. produced by our gut bacteria

    That throwaway line is doing a lot of heavy lifting. Let’s say Bacteria A is converting fibre to propionate, as well as producing Mystery Product X which prevents diabetes. But in the presence of supplemented propionate, Bacteria A’s chemical process no longer occurs, because one of the outputs already exists. So the side-effect of supplementing one seemingly innocuous chemical can be to disrupt production of another.

    I’m not a scientist, but this is well within the realms of possibility. There’s an awful lot we still don’t know about the gut microbiome.

  6. You’re not trying to do a univariate analysis on a multivariate problem there, are you

    I don’t think I am, no.

  7. Insulin is a hormone created in the pancreas in response to glucose levels in the blood stream. Its function is to help cells in muscle, fat, the liver take up glucose to be used as energy or stored.

    Anything which reduces the effectiveness of insulin will cause an increase of glucose in the blood.

    It will depend on amount of propionate consumed/produced and how much carbohydrate ingested.

    The higher the glucose level in the blood, the greater the amount of insulin produced. Therefore any effect on glucose uptake by cells caused by propionate could be countered by the increased insulin production that the increase in blood glucose levels would cause. So self levelling.

    It depends on how much propionate and other metabolic factors. Nobody knows… yet.

  8. Anything which reduces the effectiveness of insulin will cause an increase of glucose insulin in the blood.

    Fixed it for ya.

    Stop thinking univariately about multivariate problems. Especially in human physiology.

  9. Why do I suspect this is only going to be problematic to some ginormous bint in Acrington who scoffs her way through 8 Wonderloaves a day & will need major building work done to get her out her own front door and for the majority, might nibble a couple slices toased fron breakfast, it disappears in the noise which is a varied diet?
    Like the majority of diet health scares

  10. It could be a difference between gut bacteria producing whateveritis at a steady continuous trickle, and consumption being a huge spike.

  11. Maybe? Who knows for sure? Although it is curious that in the US bread has up to 2000 ppm levels of propionate and rotis and tortillas have up to 4000 ppm levels and there is a marked difference in diabetes between Latin Americans and the rest. Just sayin’.

  12. Plenty of articles saying Asians carry the biggest risk of T2 diabetes. And of this broad group the biggest risk are women who are Pakistani in origin.
    Yet there seems to be very little literature looking at exercise in this population sub-section ( I suspect it’s little to non-existent ) and a fair bit of literature about visceral fat storage, genes, blah blah.

  13. What’s the effect of cooking on propionate? Can it withstand bread baking temperatures without changing so it’s no longer the same as that produced in the gut? Just askin’ is all.

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