This news release describes results of a small, preliminary study that adds a bit more tantalizing evidence that a dietary supplement derived from a gut bacteria product may reduce appetite for high-calorie foods. The product is inulin propionate ester, a concentrated form of a compound released by normal gut bacteria when they digest a form of fiber called inulin. In turn, that compound is thought to send signals to the brain’s appetite centers that reduce food cravings.
The release, issued by Imperial College London and the University of Glasgow, does a good job of explaining how the gut-brain-satiety issues were studied in 20 human volunteers, and a decent job of framing the findings as evidence for — if not proof of — the principle that altering the gut’s microbiome can affect the regulation of appetite, food choices and possibly weight gain. But the release is much too light on quantification of the results, the limitations of functional magnetic resonance imaging (fMRI) studies and information on the 20 participants. It also omits information on any potential risks associated with the experimental supplement and the fact that an inulin powder supplement product has already made it to market.
It’s hardly news that obesity and its disease consequences are epidemic in the developed world, especially, and that any “quick and easy” method that claims to reduce cravings for the most appealing foods (sweets, carbs, etc.) would find a multitude of buyers. Research efforts that succeed in filling in details of the complex mind-brain-gut-appetite pathways are important and difficult to achieve. The research described in this release — framed by one of the investigators as “filling in a missing bit of the jigsaw” by demonstrating that the supplement decreases activity in brain areas linked to “food reward” and even “reducing the amount of food” the volunteers ate — is likely to grab attention.
But we’d also caution readers that studies involving fMRI statistical analyses have recently come under fire for questionable validity since they tend to generate a high number of false-positive results.
Granted, the study is preliminary but the release could have included an estimated cost for the supplement, particularly since a form of inulin powder is already available commercially in supplement shops and online.
We’re told by the release that participants who drank a milkshake with inulin-proprionate ester had “less” activity in areas of their brain linked to reward when shown pictures of high calorie foods. But no information is given about how much less, whether all of the participants experienced the same effect (or how many actually did and did not), or how many of the participants who drank the supplement ate 10 percent less than the control group that drank a shake with an apparently less concentrated form of inulin (the fiber) alone. Similarly, the reader is told that “overweight volunteers” who got the ester supplement daily “gained less weight” over six months, but not how much less or how overweight they were. It’s impossible to tell from the release (but it would have been very useful to know) the age and gender of the volunteers. If they were college students, for example, or mostly female, metabolic and hormonal factors might have played an outsized role in the results. Finally, references to “previous studies” were nonspecific, and did not even mention if they were animal or human studies.
Even if there were no direct harms/side effects of the supplements, it would have been useful to say so explicitly. It would also be useful to know if there’s a risk from long-term use since there was the suggestion it might have an impact on the body’s microorganisms. It also appears as if the MRI was a form of fMRI which may have carried some risks, however small.
The release gave only a sketchy description of the make-up of the study population and didn’t mention any of the specific weaknesses — or limitations — of the study methods. The published study noted that energy intake data (calories consumed) wasn’t available for a quarter of the volunteers (5 out of 20) which could limit the reliability of the measured outcomes. The study group was also limited to normal weight males. The authors noted that the study findings would need to be be confirmed in obese individuals who may have altered reward and emotional responses to food.
The release would have been stronger with some discussion on the calorie content of the milkshake whereby the supplement was delivered. The calories matter a fair bit since the study found that the supplement in the milkshake reduced consumption compared to the milkshake with just inulin by 10 percent. The study did not find that the supplement alone decreased consumption and while one might hope that it does, it can’t be deduced from this research. Other components of the milkshake and its viscosity may affect subsequent energy intake.
Does eating 10 percent less of one bowl of pasta after taking the supplement, as mentioned in the release, tell us anything meaningful about how this might work over the long term and whether it would really impact weight? The published study noted that long-term effects of inulin use are not yet known.
No mongering detected.
The release discloses funding sources.
The release notes that eating the amount of fiber to produce the same effects on the gut biome as the experimental supplement would be difficult, and notes that the average amount of daily fiber intake in the UK is just 15 grams, compared to the 60 grams that would be needed. As noted in the summary above, an alternative inulin-based product is already on the market. That would have been a useful addition to the release.
The release implicitly makes the point that the powder used in the experiment is not available to the public, but the release would have been better if this had been explicit.
The release does a good job of saying what is “new” about this particular piece of research, compared to previous studies.
The release is somewhat weakened by “omissions” of information, rather than by unjustifiable language.