Why Aspartame Isn't Scary

emmoen wrote: »

I don't not have a link I read it in my Scientific America that I have. But I didn't even think about how much was consumed

Assuming the study I found is the study to which you are referring they state the amount they supplied:

"low-dose aspartame (A, 5-7 mg/kg/d) "

That means the rats receieved 5 to 7 miligrams of aspartame per kilogram of their body weight per day. For a human that would be 400 to 560mg per day. 180mg of aspartame in the usual can of soda so you would be talking a dosage of the equivalent of 2 or 3 cans of soda per day which seems like an intake many people would likely imbibe.

What about this study did you find compelling? Or more to the point given you did not read the study itself, what about the opinion piece in scientific american that was written about this study did you find compelling?

Okay I read the paper linked here:

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0109841

Here is my summary of what they did and what their findings were in an unbiased fashion. If you doubt my summary feel free to read the paper, I linked it above.

The study was comprised of 44 Sprague-Dawly rats split into 4 test groups (so a sample size of 11 rats total per test group).

The four test groups were high-fat diet with water, high-fat diet with aspartame, standard diet with water and standard diet with aspartame. Aspartame dosage was 5-7 mg/kg/d which is equivalent to a human consuming 2-3 cans of diet soda per day. Animals were allowed to free-feed and free-drink during this time.

After 7 weeks the total amount of food and water consumed was measured and the rats weight, blood glucose, plasma insulin, plasma fatty acids and plasma insulin related gut hormone (GIP) was measured:

For whatever reason the authors displayed the results not as a CHANGE in those values from day zero but rather just the 7 week value. That makes it hard to say how much those values changed for each individual rat as there is no indication in the paper if the rats all weighed exactly the same at day zero (which is unlikely).

The results are provided in table 1.

No difference in bone mineral density was observed. Liver triglycerides were elevated in the high-fat diet group but not with aspartame. The aspartame groups drank more water (containing the aspartame) but ate less food than the other groups. Remember that they allowed these animals to free-feed as they wanted and therefore the amount or frequency they fed was not controlled at all.

Fasting blood glucose was elevated in the aspartame groups (the groups that ate less food and drank more water remember).

There was no difference between insulin-related gut hormone between groups.

Not suprisingly since the aspartame groups ate less food overall they weighed less on average at the end of the 7 weeks than the non-aspartame groups. This is actually the opposite result of what was claimed by the poster who brought up this study who said:

"There has been a study done that shows artificial sweeteners affect the bacteria in your gut. Which in turns may result in an increase absorption and resulting in weight gains and decreased production of a hormone that suppresses appetite"

At week 10 they sacrificed the animals and looked at gut microbiota composition. They found that high-fat feeding perturbed the gut microbiota with an increase in total bacteria. (because your gut microbiome is affected by eating in general). There was little difference seen between the non-aspartame groups and the aspartame groups except a slight rise in Clostridium leptum relative population.

Ratios taken of different bacteria populations between the groups showed little change between aspartame and non aspartame groups (Table 2 and Figure 2)

Blood metabolites were checked and aspartame breakdown products including aspartate methanol and phenylalanine were not elevated in the aspartame groups indicating rapid metabolism of the sweetener.

Short chain fatty acid levels showed an increase in the levels of butyrate and acetate in normal diet groups while formate and isobutyrate remained unchanged. Aspartame increased circulating propionate levels by 2.5 fold in both the normal and high fat diet groups which was the one change they recorded for aspartame (Figure 3 and Table 3)

In the discussion they list their conclusions:

"Major findings were as follows: i) APM lowered net energy consumption and body mass in both CH and HF. In HF, APM resulted in lower body fat percentage as well as a decline in plasma insulin levels; ii) APM consumption was associated with fasting hyperglycemia and impaired insulin tolerance in both CH and HF; iii) APM resulted in distinctive changes in the gut microbiota including increases in Enterobacteriaceae and Clostridium leptum. Within HF, APM attenuated typical HF-induced increases in the Firmicutes:Bacteroidetes ratio and resulted in an elevation in Roseburia ssp.; and iv) APM increased serum propionate, a SCFA of bacterial origin."

(in the text APM is aspartame). Note that they say their findings show lowered body fat percentage and lowered body mass in the aspartame groups (probably because they ate less).


What did I get from this study?

Well they didn't control at all the amount the rats ate or drank which was a major flaw in my opinion. The result of this was with the aspartame groups the rats liked the sweet water, drank more of the sweet water and therefore ate less of their food which of course had an effect on insulin resistance, the gut flora and the levels of small fatty acid chains in the blood because they ate less.

Do I think this shows that if you imbibe aspartame you will eat less? No I don't. I think it shows that in that circumstance with rats they like the sweet water and they drink more of that and eat less of their food. And that is it.

I'd be curious what the result would be if they had another control group where the water was sweetened with sugar.

Alyssa_Is_LosingIt wrote: »

Aaron_K123 wrote: »

Here is the Sci American article

http://www.scientificamerican.com/article/artificial-sweeteners-may-change-our-gut-bacteria-in-dangerous-ways/

I put it here because it was referenced but I do wish to add the caveat that scientific american is a magazine with journalists who write stories, it is not a scientific publication.

The sci american article does not reference the study directly with a citation but they mention it was last year, that it was an Israeli group and that the author was Segal. With that info it seems like the study is likely the one from the scientific journal Nature that I linked above which has Segal as one of its authors.

Thanks for the overview. That was an interesting read.

Hah, thanks. I know this makes me a bit of a pain in the a** but I feel fairly strongly that if you are going to reference to some source you need to be able to present that source so that others are free to evaluate it for themselves. If you do not have a link to the original source and you still want to refer to it you should just replace the name of the source with "my cousin Ted".

So for example:

"I read an article in a scientific journal that said that aspartame causes cancer!" (no citation provided)

becomes:

"My cousin Ted said that aspartame causes cancer!"

because if you do not cite, then it is akin to heresay and you may as well present it as such.

The reason for this is because you are denying others the ability to look at your source critically and forcing them to rely solely on your personal interpretation of it.

And yes I realize holding people to this standard makes me a bit of an a**hole but I think if you want to state your case and attempt to support it with evidence from external sources you can at least be bothered to provide said external source as a matter of common courtesy or intellectual honesty.