Why?

From the linked study:

Editor’s summary
Excess dietary intake of fructose can lead to hepatic lipid accumulation and the development of steatotic liver disease. In zebrafish, Jackstadt et al. found that dietary glucose was converted to sorbitol in the intestine, which was subsequently converted to fructose in the liver in the absence of gut microbiota. Antibiotic treatment of zebrafish to deplete gut microbiota resulted in hepatic steatosis, an effect mimicked by high concentrations of exogenous sorbitol and attenuated by inhibiting sorbitol formation or by intestinal repopulation with sorbitol-degrading Aeromonas bacteria. These results indicate that sorbitol is derived from glucose in the zebrafish intestine, implicate gut microbiota in protecting against sorbitol-induced steatosis, and suggest that dietary sorbitol, which is used as a sugar substitute, may increase the risk of developing steatotic liver disease. —Wei Wong

Abstract
Metabolic dysfunction–associated steatotic liver disease (MASLD) is linked to a shift in the composition of the gut microbiome. Here, we found that depletion of the gut microbiome in adult zebrafish led to the development of steatotic liver disease in animals on standard diets. Using metabolomics and isotope tracing, we found that dietary glucose was converted to sorbitol by host intestinal cells. Although bacteria degraded sorbitol in control animals, sorbitol was transferred to the livers of fish when the gut microbiome had been depleted. Within the liver, sorbitol was converted into fructose 1-phosphate, which subsequently activated glucokinase and increased glycolytic flux, leading to increased hepatic glycogen and fat content. Inhibition of sorbitol production in microbiome-depleted animals was sufficient to prevent the development of steatotic liver, and colonizing the intestines of microbiome-depleted fish with sorbitol-degrading Aeromonas bacterial strains rescued the steatotic liver phenotype. Conversely, exogenous administration of high concentrations of sorbitol phenocopied gut microbiota depletion and induced hepatic steatosis. Together, these findings show that sorbitol-degrading bacteria in the gut protect against steatotic liver disease and suggest that excessive intake of dietary sorbitol may pose a risk for the development of MASLD.

They’re implicating several types of natural sugars and saying that if you killed your gut microbiome with high concentration of sorbitol, then it might be bad for your liver. Ok??? Without any indication of the human-equivalent amounts involved, this is utterly useless. And this from a team who already went “HFCS feeds cancer!”? Seems like headline-chasers to me.

Also, since I read this earlier today:

The UK’s Scientific Advisory Committee on Nutrition in 2015 disputed the claims of fructose causing metabolic disorders, stating that “there is insufficient evidence to demonstrate that fructose intake, at levels consumed in the normal UK diet, leads to adverse health outcomes independent of any effects related to its presence as a component of total and free sugars.”[60]

I usually don’t bother answering a Gish Gallop, but…

1 - They didn’t complete the study, it was only 13 people with an existing history of mental disorders

2 - They basically said it’s so within the tolerances that it’s probably just chance, and that regular soda did as bad or worse

3 - Could only get the abstract, and it says nothing about their findings

4 - Combines aspartame and acesulfame-K, so it’s hard to tell from the abstract. The methodology doesn’t fill me with a lot of hope for it though.

5 - Seems to be the same study as 4 (same group of French people, same author), but for cardiovascular disease instead of cancer? Which, yeah, fat people drink diet soda, have heart disease, and get cancer more than thin people. I’m not sold on their methodology

6 - It’s a rat study. Again, I can’t see anything but the abstract, so it’s hard to say. But any study that doesn’t do a comparative analysis against regular sugar is suspect in my book

7 - Like 2, this one says that it’s probably just chance in the conclusion.

And look, if this was some new chemical on the block, maybe I’d agree that it should have some more testing. But it’s aspartame. It’s been being actively studied since 1965. It’s had a lot of negative PR backed by Domino (et al), which has created a huge amount of public concern. And will all of that, the studies still come out a hundred to one that there’s not really any link to anything.

Yes, you can find studies that say “aspartame scary.” But they’re basically like all the ones you linked above. Dubious. Most even admit they’re dubious (as seen above). And almost none of the ones that push the “scary” rhetoric compare the effects against regular table sugar, which is also heavily linked to increased cancer/heart disease risk. So it’s not even intellectually honest, even when their numbers happen to random out to slightly agreeing with them.

I just opened up the last link and it took me 5 seconds to find this:

Rats that had received aspartame (1000 mg/kg b.wt.)

One liter of coke zero has 240mg of aspartame.

https://juiceradvices.com/how-much-aspartame-is-in-coke-zero/

1000mg per kg would mean, in a human with, let’s say 80kg, we’d need 80000mg to replicate the study case.

Since we - usually - don’t eat pure aspartame, that would mean you’d need to chug 333.33 liters of diet coke per day to replicate the aspartame intake of the rats in the study.

These studies are so far off of reality that I barely know where to begin.

I asked chatGPT and it said not to believe you because your links won’t even open