Why Aspartame Isn't Scary

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  • Wheelhouse15
    Wheelhouse15 Posts: 5,575 Member
    Aaron_K123 wrote: »
    In terms of the methanol component let me use an analogy. Lets pretend that rather than aspartame orally the rats were just given methanol directly. Lets also treat methanol as just alcohol consumption which is fair because it is alcohol. So the rats were given alcohol once daily in one bulk amount. They were given a certain amount per day each day for 90 days.

    After 90 days the amount of alcohol was measured in their blood and the amount was 8 times higher than the amount that they were given each day.

    If that is how blood alcohol content worked that would mean if you drank one beer in a sitting per day that on the 8th day you'd be drunk and not only that but if you continued to drink one beer a day you would be drunk 24/7 for the next 82 days.

    That seems a bit odd to me. I'm going to look up the type of rats they used in the study, see if they have any impaired liver function or something. EDIT: nope, just the Wistar rats...so fairly normal. Are rats just crap at alcohol metabolism?

    According to the study they metabolize it immediately in the liver with folic acid, which was why I question how well the MTX mimics humans who have that anti-oxidant available.
  • Aaron_K123
    Aaron_K123 Posts: 7,122 Member
    Wheelhouse15 wrote: »
    Aaron_K123 wrote: »
    In terms of the methanol component let me use an analogy. Lets pretend that rather than aspartame orally the rats were just given methanol directly. Lets also treat methanol as just alcohol consumption which is fair because it is alcohol. So the rats were given alcohol once daily in one bulk amount. They were given a certain amount per day each day for 90 days.

    After 90 days the amount of alcohol was measured in their blood and the amount was 8 times higher than the amount that they were given each day.

    If that is how blood alcohol content worked that would mean if you drank one beer in a sitting per day that on the 8th day you'd be drunk and not only that but if you continued to drink one beer a day you would be drunk 24/7 for the next 82 days.

    That seems a bit odd to me. I'm going to look up the type of rats they used in the study, see if they have any impaired liver function or something. EDIT: nope, just the Wistar rats...so fairly normal. Are rats just crap at alcohol metabolism?

    According to the study they metabolize it immediately in the liver with folic acid, which was why I question how well the MTX mimics humans who have that anti-oxidant available.

    So if methanol is metabolized "immediately" then how does methanol end up at levels 8 times higher than the daily administered dose within the blood? From my (now correct) math 3.88mg extra total in the blood of the aspartame group who are recieving 8.4mg of aspartame daily which with perfect metabolic conversion and uptake would be at most 0.84mg of methanol into the blood daily.
  • Wheelhouse15
    Wheelhouse15 Posts: 5,575 Member
    edited November 2016
    Aaron_K123 wrote: »
    Wheelhouse15 wrote: »
    Aaron_K123 wrote: »
    In terms of the methanol component let me use an analogy. Lets pretend that rather than aspartame orally the rats were just given methanol directly. Lets also treat methanol as just alcohol consumption which is fair because it is alcohol. So the rats were given alcohol once daily in one bulk amount. They were given a certain amount per day each day for 90 days.

    After 90 days the amount of alcohol was measured in their blood and the amount was 8 times higher than the amount that they were given each day.

    If that is how blood alcohol content worked that would mean if you drank one beer in a sitting per day that on the 8th day you'd be drunk and not only that but if you continued to drink one beer a day you would be drunk 24/7 for the next 82 days.

    That seems a bit odd to me. I'm going to look up the type of rats they used in the study, see if they have any impaired liver function or something. EDIT: nope, just the Wistar rats...so fairly normal. Are rats just crap at alcohol metabolism?

    According to the study they metabolize it immediately in the liver with folic acid, which was why I question how well the MTX mimics humans who have that anti-oxidant available.

    So if methanol is metabolized "immediately" then how does methanol end up at levels 8 times higher than the daily administered dose within the blood? From my (now correct) math 3.88mg extra total in the blood of the aspartame group who are recieving 8.4mg of aspartame daily which with perfect metabolic conversion and uptake would be at most 0.84mg of methanol into the blood daily.

    The MTX made them folic deficient so that the methanol was free to enter the blood stream without formating in liver as normal (this is actually right from the study, which is why I think it's a great read in general). This is supposed to mimic human metabolism, but as I noted with some primate studies, folic acid can be used to alleviate the symptoms of -- you guessed it -- methanol toxicity.

    How they ended up with a higher amount than should have been expected when accounting for the control group levels is something I'm not sure of. Mice might generate there own methanol and it might be influenced by the aspartame? This bears investigation. I would like to see why this might end up with something like a 5% increase over expected values.
  • Aaron_K123
    Aaron_K123 Posts: 7,122 Member
    Wheelhouse15 wrote: »
    Aaron_K123 wrote: »
    Wheelhouse15 wrote: »
    Aaron_K123 wrote: »
    In terms of the methanol component let me use an analogy. Lets pretend that rather than aspartame orally the rats were just given methanol directly. Lets also treat methanol as just alcohol consumption which is fair because it is alcohol. So the rats were given alcohol once daily in one bulk amount. They were given a certain amount per day each day for 90 days.

    After 90 days the amount of alcohol was measured in their blood and the amount was 8 times higher than the amount that they were given each day.

    If that is how blood alcohol content worked that would mean if you drank one beer in a sitting per day that on the 8th day you'd be drunk and not only that but if you continued to drink one beer a day you would be drunk 24/7 for the next 82 days.

    That seems a bit odd to me. I'm going to look up the type of rats they used in the study, see if they have any impaired liver function or something. EDIT: nope, just the Wistar rats...so fairly normal. Are rats just crap at alcohol metabolism?

    According to the study they metabolize it immediately in the liver with folic acid, which was why I question how well the MTX mimics humans who have that anti-oxidant available.

    So if methanol is metabolized "immediately" then how does methanol end up at levels 8 times higher than the daily administered dose within the blood? From my (now correct) math 3.88mg extra total in the blood of the aspartame group who are recieving 8.4mg of aspartame daily which with perfect metabolic conversion and uptake would be at most 0.84mg of methanol into the blood daily.

    The MTX made them folic deficient so that the methanol was free to enter the blood stream without formating in liver as normal (this is actually right from the study, which is why I think it's a great read in general). This is supposed to mimic human metabolism, but as I noted with some primate studies, folic acid can be used to alleviate the symptoms of -- you guessed it -- methanol toxicity.

    How they ended up with a higher amount than should have been expected when accounting for the control group levels is something I'm not sure of. Mice might generate there own methanol and it might be influenced by the aspartame? This bears investigation. I would like to see why this might end up with something like a 5% increase over expected values.

    Aspartame is metabolically broken down into two common amino acids and methanol. So if aspartame "influences" methanol buildup it would have to be due to those common amino acids which would imply that protein would cause the same build-up which strikes me as unlikely. Not sure how that would even work to be honest.

    Do you have a science background, you seem like it?
  • Wheelhouse15
    Wheelhouse15 Posts: 5,575 Member
    Aaron_K123 wrote: »
    Wheelhouse15 wrote: »
    Aaron_K123 wrote: »
    Wheelhouse15 wrote: »
    Aaron_K123 wrote: »
    In terms of the methanol component let me use an analogy. Lets pretend that rather than aspartame orally the rats were just given methanol directly. Lets also treat methanol as just alcohol consumption which is fair because it is alcohol. So the rats were given alcohol once daily in one bulk amount. They were given a certain amount per day each day for 90 days.

    After 90 days the amount of alcohol was measured in their blood and the amount was 8 times higher than the amount that they were given each day.

    If that is how blood alcohol content worked that would mean if you drank one beer in a sitting per day that on the 8th day you'd be drunk and not only that but if you continued to drink one beer a day you would be drunk 24/7 for the next 82 days.

    That seems a bit odd to me. I'm going to look up the type of rats they used in the study, see if they have any impaired liver function or something. EDIT: nope, just the Wistar rats...so fairly normal. Are rats just crap at alcohol metabolism?

    According to the study they metabolize it immediately in the liver with folic acid, which was why I question how well the MTX mimics humans who have that anti-oxidant available.

    So if methanol is metabolized "immediately" then how does methanol end up at levels 8 times higher than the daily administered dose within the blood? From my (now correct) math 3.88mg extra total in the blood of the aspartame group who are recieving 8.4mg of aspartame daily which with perfect metabolic conversion and uptake would be at most 0.84mg of methanol into the blood daily.

    The MTX made them folic deficient so that the methanol was free to enter the blood stream without formating in liver as normal (this is actually right from the study, which is why I think it's a great read in general). This is supposed to mimic human metabolism, but as I noted with some primate studies, folic acid can be used to alleviate the symptoms of -- you guessed it -- methanol toxicity.

    How they ended up with a higher amount than should have been expected when accounting for the control group levels is something I'm not sure of. Mice might generate there own methanol and it might be influenced by the aspartame? This bears investigation. I would like to see why this might end up with something like a 5% increase over expected values.

    Aspartame is metabolically broken down into two common amino acids and methanol. So if aspartame "influences" methanol buildup it would have to be due to those common amino acids which would imply that protein would cause the same build-up which strikes me as unlikely. Not sure how that would even work to be honest.

    Do you have a science background, you seem like it?

    Yeah, I'm just trying to provide very generous answer without casting suspicious glances lol.

    Neuroscience degree so a bit of micro bio and biochem where involved in ways that I'm almost completely recovered from after long therapy sessions! ;) I'm not particularly well versed in mouse physiology but I did see a ton of studies like this, along with those giant squid axons! ;)
  • AnvilHead
    AnvilHead Posts: 18,343 Member
    Aaron_K123 wrote: »
    In terms of the methanol component let me use an analogy. Lets pretend that rather than aspartame orally the rats were just given methanol directly. Lets also treat methanol as just alcohol consumption which is fair because it is alcohol. So the rats were given alcohol once daily in one bulk amount. They were given a certain amount per day each day for 90 days.

    After 90 days the amount of alcohol was measured in their blood and the amount was 8 times higher than the amount that they were given each day.

    If that is how blood alcohol content worked that would mean if you drank one beer in a sitting per day that on the 8th day you'd be drunk and not only that but if you continued to drink one beer a day you would be drunk 24/7 for the next 82 days.

    That seems a bit odd to me. I'm going to look up the type of rats they used in the study, see if they have any impaired liver function or something. EDIT: nope, just the Wistar rats...so fairly normal. Are rats just crap at alcohol metabolism?

    A lot of the other math you guys are doing is over my head (although very interesting), but I can contribute to the bolded. The human body metabolizes ethyl alcohol at a rate of around .02% per hour (I believe this figure was given for a 150-pound person). So if a 150 pound person drank a bolus of 4 oz. of alcohol resulting in a BAC of 0.08%, then quit drinking, that ETOH would be completely oxidized/eliminated within the next 4 hours. If the same bolus was administered on the next day, their blood alcohol would again be back to 0.00% within 4 hours. And so on. The effect is not cumulative.

    I'm not sure how (or if) that correlates to rats, as I'm not familiar with the drinking habits or alcohol metabolism rates of rats.
  • Jeannie3099
    Jeannie3099 Posts: 61 Member
    Face it, it's nasty stuff. I'm losing and I include a little sugar, butter and all the real stuff. Won't risk any health concerns with aspartame. Or fake fat. I took in a lot of the sugar substitute once a long time ago and did not lose weight. I got hungrier! My ears also started ringing. Why mess with your body like that?
  • GottaBurnEmAll
    GottaBurnEmAll Posts: 7,722 Member
    stevencloser wrote: »
    GottaBurnEmAll wrote: »
    I just want to express my continuing appreciation for this thread. I've learned a lot from it, and the sciencey conversations are fascinating.

    Almost as fascinating as people who apparently don't read a single post of the thread, not even OP, chiming in.

    Those posts are pure entertainment.
  • stealthq
    stealthq Posts: 4,298 Member
    edited November 2016
    Totally cribbing this from an overview of a study comparing methanol metabolism in mice vs. primates (linked below) that I have not read in depth. But, I thought it may help clear up the questions on methanol buildup:

    "The mouse model for human developmental toxicity of methanol is contentious because of the differences in formate oxidation. However, human exposures to environmental methanol are unlikely to produce blood levels saturating this pathway, so formate buildup would be unlikely; indeed, monkeys exposed to 2000 ppm showed no formate accumulation. Thus, methanol rather than formate may be the proximate toxicant in humans, and in the mouse higher exposures of methanol can be studied without formate accumulation. Oxidation of methanol by catalase in mice vs. ADH in humans may also be important."

    https://cfpub.epa.gov/si/si_public_record_Report.cfm?dirEntryId=153763&CFID=81868876&CFTOKEN=70698412
  • Aaron_K123
    Aaron_K123 Posts: 7,122 Member
    stealthq wrote: »
    Totally cribbing this from an overview of a study comparing methanol metabolism in mice vs. primates (linked below) that I have not read in depth. But, I thought it may help clear up the questions on methanol buildup:

    "The mouse model for human developmental toxicity of methanol is contentious because of the differences in formate oxidation. However, human exposures to environmental methanol are unlikely to produce blood levels saturating this pathway, so formate buildup would be unlikely; indeed, monkeys exposed to 2000 ppm showed no formate accumulation. Thus, methanol rather than formate may be the proximate toxicant in humans, and in the mouse higher exposures of methanol can be studied without formate accumulation. Oxidation of methanol by catalase in mice vs. ADH in humans may also be important."

    https://cfpub.epa.gov/si/si_public_record_Report.cfm?dirEntryId=153763&CFID=81868876&CFTOKEN=70698412

    There is often differences between mice and rats in terms of small molecule metabolism as well and the study in question was done in rats. I know mice have considerably different cyp P450s so their metabolic profile for small molecules can be quite different than rats or humans. Although cyp P450s I don't think are involved in methanol metabolism.
  • leanjogreen18
    leanjogreen18 Posts: 2,492 Member
    It's been said...

    If you're the smartest person in the room, you're in the wrong room.

    Welp I'm def in the right room:).
  • cerise_noir
    cerise_noir Posts: 5,468 Member
    snickerscharlie wrote: »
    Just want to chime in and say science geeks are sexay. <3

    I've learned so much from this thread.

    Right?!! I adore threads such as this.
  • leeannek1
    leeannek1 Posts: 16 Member
    Wow thanks for sharing! Good to know! I thought aspartame was the devil.:)
  • leanjogreen18
    leanjogreen18 Posts: 2,492 Member
    So it may not be scarey but does it prevent weight loss? Need help interpreting.

    https://www.sciencedaily.com/releases/2016/11/161122193100.htm
  • Wheelhouse15
    Wheelhouse15 Posts: 5,575 Member
    edited November 2016
    johunt615 wrote: »
    So it may not be scarey but does it prevent weight loss? Need help interpreting.

    https://www.sciencedaily.com/releases/2016/11/161122193100.htm

    The mechanism might hold but the key is one of the essential amino acids (Phenylalanine) that is found in much higher amounts in various proteins that are found in meats, milk etc. so again we are left with a case where we can show something in mice but how relevant is it to us?

    So do we eliminate all sources of Phenylalanine? Probably not a good idea but there is a medical disorder that requires strict control of intake (PKU) and deficiencies can have really serious side effects.

    ETA: two interesting statements:

    "In a 2013 study published in Proceedings of the National Academy of Sciences, Hodin's team found that feeding IAP to mice kept on a high-fat diet could prevent the development of metabolic syndrome and reduce symptoms in animals that already had the condition. Phenylalanine is known to inhibit the action of IAP, and the fact that phenylalanine is produced when aspartame is digested led the researchers to investigate whether its inhibitory properties could explain aspartame's lack of a weight-loss effect."

    "At the end of the study period, while there was little difference between the weights of the two groups fed a normal diet, mice on a high-fat diet that received aspartame gained more weight than did those on the same diet that received plain water. Aspartame-receiving mice in both diet groups had higher blood sugar levels than did those fed the same diets without aspartame, which indicates glucose intolerance, and both aspartame-receiving groups had higher levels of the inflammatory protein TNF-alpha in their blood, which suggests the kind of systemic inflammation associated with metabolic syndrome."

    Later it talks about increase in caloric consumption for people who consume drinks with aspartame. So did they allow eating ad Librium? Probably the real issue but there was no discussion of holding calories constant that I could see in this article. So why did the rats on the normal diet with aspartame not experience the weight gain of the high fat diet rats when a high fat diet was supposed to provide relief against metabolic syndrome such as this? Also, not sure why both groups would exhibit markers of metabolic system in their blood work but only the high fat group actually manifested this in weight gain as should be expected. Seems like we might have some funny business going on. I'd have to see some confirmation since this type of sleight of hand is becoming common place in research it seems.
  • Wheelhouse15
    Wheelhouse15 Posts: 5,575 Member
    edited November 2016
    johunt615 wrote: »
    So it may not be scarey but does it prevent weight loss? Need help interpreting.

    https://www.sciencedaily.com/releases/2016/11/161122193100.htm

    Found this link to another article that might be the one mentioned above regarding high fat diets: https://www.sciencedaily.com/releases/2013/04/130408152902.htm. It seems that you have to administer IAP*, what Phenylalanine is supposed to inhibit or else you get an increase in metabolic syndrome, which might explain why only the high fat diet had those issues in this study. One might conclude that this is the reason why it's not carbs but weight gain in general that leads to metabolic syndrome manifestations such as type 2 diabetes but that's drawing upon inferences on my part.

    Perhaps only those on high fat diets need to worry about aspartame? This is still pretty new research and hard to see how this applies to humans who aren't research subjects.

    *The chain of events seems to be that IAP blocks LPS, and it's LPS which can lead to low grade inflammation associated with metabolic syndrome. LPS enters the blood stream on fat so inhibiting LPS reduces this.
  • stealthq
    stealthq Posts: 4,298 Member
    Aaron_K123 wrote: »
    stealthq wrote: »
    Totally cribbing this from an overview of a study comparing methanol metabolism in mice vs. primates (linked below) that I have not read in depth. But, I thought it may help clear up the questions on methanol buildup:

    "The mouse model for human developmental toxicity of methanol is contentious because of the differences in formate oxidation. However, human exposures to environmental methanol are unlikely to produce blood levels saturating this pathway, so formate buildup would be unlikely; indeed, monkeys exposed to 2000 ppm showed no formate accumulation. Thus, methanol rather than formate may be the proximate toxicant in humans, and in the mouse higher exposures of methanol can be studied without formate accumulation. Oxidation of methanol by catalase in mice vs. ADH in humans may also be important."

    https://cfpub.epa.gov/si/si_public_record_Report.cfm?dirEntryId=153763&CFID=81868876&CFTOKEN=70698412

    There is often differences between mice and rats in terms of small molecule metabolism as well and the study in question was done in rats. I know mice have considerably different cyp P450s so their metabolic profile for small molecules can be quite different than rats or humans. Although cyp P450s I don't think are involved in methanol metabolism.

    Methanol metabolism is very similar for mice and rats as far as using catalase vs. ADH in humans. Obviously, there can always be differences in the kinetics given the enzymes are likely orthologous and not identical in amino acid sequence.
  • Wheelhouse15
    Wheelhouse15 Posts: 5,575 Member
    edited November 2016
    stealthq wrote: »
    Aaron_K123 wrote: »
    stealthq wrote: »
    Totally cribbing this from an overview of a study comparing methanol metabolism in mice vs. primates (linked below) that I have not read in depth. But, I thought it may help clear up the questions on methanol buildup:

    "The mouse model for human developmental toxicity of methanol is contentious because of the differences in formate oxidation. However, human exposures to environmental methanol are unlikely to produce blood levels saturating this pathway, so formate buildup would be unlikely; indeed, monkeys exposed to 2000 ppm showed no formate accumulation. Thus, methanol rather than formate may be the proximate toxicant in humans, and in the mouse higher exposures of methanol can be studied without formate accumulation. Oxidation of methanol by catalase in mice vs. ADH in humans may also be important."

    https://cfpub.epa.gov/si/si_public_record_Report.cfm?dirEntryId=153763&CFID=81868876&CFTOKEN=70698412

    There is often differences between mice and rats in terms of small molecule metabolism as well and the study in question was done in rats. I know mice have considerably different cyp P450s so their metabolic profile for small molecules can be quite different than rats or humans. Although cyp P450s I don't think are involved in methanol metabolism.

    Methanol metabolism is very similar for mice and rats as far as using catalase vs. ADH in humans. Obviously, there can always be differences in the kinetics given the enzymes are likely orthologous and not identical in amino acid sequence.

    I liked your crib notes on the differences between primates and lab mice and rats because I had similar concerns when I was looking up some of the methanol and folate studies on chimps. If you have to induce folate deficiency in mice in order to allow methanol to pass into the blood stream to mimic humans then you are also taking away the what is likely the primary anti-oxidant that binds on the free radicals that are the culprits in the observed oxidation stress on the CNS. So the study linked probably resolves the first issue of the differnt mechanism of methanol toxicity between mice and men (had to do that!) but now has likely introduced a confounding variable of removal of the primary anti-oxidant that is used to alleviate the effects. This is just thinking out loud, but certainly something I think warrants further investigation to answer.

    Now I need more therapy! ;)
  • leanjogreen18
    leanjogreen18 Posts: 2,492 Member
    Thanks Wheelhouse15!!!

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