Diet Soda and other nutrition related stuff

TheTom

Member
Diet Soda

What are your guys opinions on Diet Soda while on a cut? I've just started drinking a lot of Diet Dr Pepper Cherry Vanila and Diet Pepsi Lime, for the caffeine and taste. I actually enjoy the taste more than normal pop, cause I'm not too big on things that are overly sweet.

But it seems a little too good to be true? I mean 0carb 0fat +caffeine, with instant sugar/hunger appetite suppression, there has to be SOMETHING wrong with it.

Is there some kind of extreme insulin spike? It's just hard for me to believe I'm drinking all this pop and my cutting isn't being affected at all, it's frickin great.
 
you should be alright and not have problems from the diet sodas. Although many people believe that carbonated drink basically lower the protein absorption. I have never seen any studies for this, but it should be negligible if it indeed happens. Try the sugar free crystal light, awesome.
 
down south, in texas anyway, people refer to all sodas as "coke." Just what i'm told anyway. I am happy to say i'm north of texas.
 
knox said:
down south, in texas anyway, people refer to all sodas as "coke." Just what i'm told anyway. I am happy to say i'm north of texas.
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Yes sir, deep south Texas especially, where I reside, its referred as coke. Confusing in a border town lol :drunk:
 
aristotle said:
Yes sir, deep south Texas especially, where I reside, its referred as coke. Confusing in a border town lol :drunk:
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you ain't lying. around here all those texans say they want coke and expect you to ask them what kind. They don't seem to understand that coke is a brand...lol.
 
dsl said:
you ain't lying. around here all those texans say they want coke and expect you to ask them what kind. They don't seem to understand that coke is a brand...lol.
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What you don't get is when you get down deep enough, there is no other brand. :) Try and find a Pepsi machine in Atlanta. Heh. There are parts of town where EVERYTHING is named after a Woodruff or one of the other Coke men.

Funny all the variations.

The people who really crack me up are the ones who say "teeter totter." No, it's a "see saw," nitwit! ;)
 
jmh80 said:
Pop - you must be from up north.
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Most of the northeast says soda. In NY, east of Rochester says soda, while Rochester westward says pop.

I'm from Syracuse and when people say pop it's like nails on a chalkboard.

/karp
 
I am from Jersey, like 5 minutes from NYC and we city boys say SODA! Pop seems so weird and when we say coke we mean Coca-Cola!
 
pop is fag dancers like nsync. Coke is what all soda's are called, you then specify what type you want.
 
i remember one time my friends and i were in dallas and we stopped to eat. When i told the waitress i wanted a coke and she asked me what kind, i just wanted to punch her right in the ovaries...:lol:. Jeez, there's only one kind.
 
in Kansas the majority use pop. I do hear soda used sometimes. But in kansas pop, milk, water, or beer can be confused with whiskey....lol
 
BOHICA said:
pop is fag dancers like nsync. Coke is what all soda's are called, you then specify what type you want.
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You see, Coke is a brand. It would be like going to a car dealership, asking for a Beatle, and then being upset when he only showed you Beatles. "I was thinking something more along the lines of an SUV type Beatle." WTF?

If anyone ever asks me "what kind" when I ask for a coke or diet coke, I would have to be like "What kind? What do you mean what kind? Go get me a fucking coke."
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In Boston we call it soda, but for some reason most Bostonians say So-der. Weird. They drop the r where it should be, as in "cah", but add it where it doesn't belong, "idear". Not the sharpest lot around here. It actually comes down to a laziness of pronounciation. If you pay attention to the different pronounciations you'll notice that it is easier to leaver car "open", "cah". OTOH, pronouncing two consecutive long vowels (idea) is more complicated then one short followed by a consonant...hence "idear". For some reason I don't have a Boston accent despite having lived here my whole life. Maybe it has to do with the fact that I think about **** like what I just posted.
 
Qwerty said:
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That looks like Dr. Pepper or Pepsi in that glass. I guess you didn't specify what kind of coke you wanted.

Coke (with a capital C) is the brand, coke is the name for all "pop" :)
 
BOHICA said:
That looks like Dr. Pepper or Pepsi in that glass. I guess you didn't specify what kind of coke you wanted.

Coke (with a capital C) is the brand, coke is the name for all "pop" :)
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Oh, good. So when you ask for soda, you say, "I would like some coke, with a little c, specifically a Dr. Pepper."[you know, since noone can tell if you are capitalizing it when you talk, and coke is a brand name].

"I would like to buy a beatle, specifically a Chevy Avalanche."

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This thread has been officially hijacked, lol.
 
:icon_lol:

this thread is making me thirsty. I think i'm go get some coke with a capital C.
 
TheTom said:
What are your guys opinions on Diet Soda while on a cut? I've just started drinking a lot of Diet Dr Pepper Cherry Vanila and Diet Pepsi Lime, for the caffeine and taste. I actually enjoy the taste more than normal pop, cause I'm not too big on things that are overly sweet.

But it seems a little too good to be true? I mean 0carb 0fat +caffeine, with instant sugar/hunger appetite suppression, there has to be SOMETHING wrong with it.

Is there some kind of extreme insulin spike? It's just hard for me to believe I'm drinking all this pop and my cutting isn't being affected at all, it's frickin great.
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No extreme insulin spike. In the absence of a large influx of glucose that could be quite fatal.

About the only thing I can think of is acidity on the teeth and long term effects of artificial sweeteners. So enjoy!

Oh yeah - just call the drink by its damn name.
 
Nitrox said:
No extreme insulin spike. In the absence of a large influx of glucose that could be quite fatal.

About the only thing I can think of is acidity on the teeth and long term effects of artificial sweeteners. So enjoy!

Oh yeah - just call the drink by its damn name.
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Alot of people in the south refer to soda as just "drink" which is incredibly stupid. Anyway I think that FRESCA is the answer to this debate. Every can of Fresca says " A Crisp Grapefruit Flavored SODA." Yes folks it soda. Not drink, coke, pop, but SODA.
 
Nitrox said:
No extreme insulin spike. In the absence of a large influx of glucose that could be quite fatal.

About the only thing I can think of is acidity on the teeth and long term effects of artificial sweeteners. So enjoy!
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If you go over to BB.com (gasp!), under the nutrition forum they have a sticky about the health effects of artificial sweeteners. It has study after study after study claiming that there is no long term health risks so I guess you might even not have to worry about that.

EDIT: god d*mn I can't spell
 
bullydog said:
If you go over to BB.com (gasp!), under the nutrition forum they have a sticky about the health effects of artificial sweeteners. It has study after study after study claiming that there is no long term health risks so I guess you might even not have to worry about that.

EDIT: god d*mn I can't spell
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So just want to make sure of this.... there's no problem having a diet coke? (notice the little c) Excellent!
 
3v1l said:
So just want to make sure of this.... there's no problem having a diet coke? (notice the little c) Excellent!
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None at all, especially if had in moderation.
 
Beowulf said:
In Boston we call it soda, but for some reason most Bostonians say So-der. Weird. They drop the r where it should be, as in "cah", but add it where it doesn't belong, "idear". Not the sharpest lot around here. It actually comes down to a laziness of pronounciation. If you pay attention to the different pronounciations you'll notice that it is easier to leaver car "open", "cah". OTOH, pronouncing two consecutive long vowels (idea) is more complicated then one short followed by a consonant...hence "idear". For some reason I don't have a Boston accent despite having lived here my whole life. Maybe it has to do with the fact that I think about **** like what I just posted.
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I don't have a rhode island accent despite having grown up there. all I can say is... THANK FUCKING GOD.
 
exnihilo said:
I don't have a rhode island accent despite having grown up there. all I can say is... THANK FUCKING GOD.
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:icon_lol:


The Rhode Island accent sounds to me like a cross between Boston and NY.
 
Well, where I'm at we call "having a beer" either "having a pop", or a "road coke."

By the way, try the Diet Coke with Splenda. :thumbsup:
 
just tried it the other day .

tasted like pepsi :rasp:.

so despite that it's better for you.
i'm staying with regular diet coke vanilla.
 
Pop? what is this 1950. :frustrate That's like people where I live saying they have on "tennis Shoes". They all call any sneaker whether it be basketball, running or whatever, tennis shoes. I go nutz daily saying I'm wearing running shoes damit I don't play tennis, they don't get it. :rant:
 
Originally Posted by jminis
Pop? what is this 1950. Invalid Link Removed That's like people where I live saying they have on "tennis Shoes". They all call any sneaker whether it be basketball, running or whatever, tennis shoes. I go nutz daily saying I'm wearing running shoes damit I don't play tennis, they don't get it. Invalid Link Removed
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I never heard soda referred to as "pop" until I came to the midwest. "Tennis shoes" either. I'm from Brooklyn (duh) and everyone there uses, I don't know, the actual name of things to ask for them. We call soda by brand name, sneakers "a pair of sneakers" or "a pair of *insert brand name*'s" and we don't "worsh" our clothes either. Fuggeddaboutit! lol I don't think Michael Jordan ever used a pair of "Air Tennis Shoes" to win an NBA championship.

On a more serious note, the question was asked about diet soda. I posted this earlier in another thread:

What's wrong with aspartame?

Aspartame a.k.a. NutraSweet is a neurotoxic posion. It breaks down on the shelf or in the human body into several toxins and the amino acid d-phenylalanine. Those toxins being formaldehyde, methanol, formic acid and diketobenzaprine (DKP). Formaldehyde, boys and girls, is embalming fluid. Not too nice to the human body. Methanol is a wood alcohol which is present in aspartamein large amounts. In aspartame, it breaks down into formaldehyde and formic acid (fire ant venom). The FDA recommends a limit of 7.8 mg/day of methanol. A quart of aspartame-sweetened beverage contains about 56 mg methanol. DKP has been shown to cause brain cancer in lab rats. Furthermore, d-phenylalanine as present in aspartame is a free excitotoxin with similar effects to the amino in monosodium glutamate (d-glutamic acid). An excitotoxin is a chemical which can penetrate the brain barrier upon digestion in large amounts. When it reaches the brain, it causes overstimulation of the brain's neurons, so that they become very excited to the point of cell death. It's like forcing 100 watts of power through a 60 watt light bulb. Like little xmas lights on the brain, its neurons flicker faster and brighter until they burn out. Aspartame and MSG-like substances have been linked to major neurological disorders such as Multiple Sclerosis, Parkinson's Disease, Alzheimer's and Fibromyalgia, as well as numerous physical problems including macular degeneration, digestive issues and in an ironic twist, gross obesity. Some persons are more sensitive to feeling the effects of these substances than others, but they effect everyone to some degree as they are poisons, not allergens.
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A 35 year ADA member, world famous diabetic specialist H.J.Roberts, M.D., discovered aspartame can precipitate diabetes and reacts harmfully with insulin.
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The only reason aspartame was ever approved was that the only studies the FDA used when they unbanned it were written by the company that made aspartame, which was headed by a certain Donald Rumsfeld.
 
I'm not saying the above post is wrong, but I doubt the effects of aspartame are anywhere near as damaging as the article would like you to believe.

I have many friends who compete in the NPC junior division up here in the NW and most of them swear by diet soda and drink it by the liter. Not only that, but come competition time, they get down to 3%-5% bodyfat, while doing so.

I myself have just started drinking it about a month or so ago, on a regular basis, and haven't noticed any ill effects from it. Except that it kills my cravings for sweets, blunts my appetite and the extra caffeine keeps me alert, leaner and dryer looking.
 
I myself have just started drinking it about a month or so ago, on a regular basis, and haven't noticed any ill effects from it.
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Most people do not feel short term effects of aspartame, or they attribute them to something else. It's similar to MSG in that a specific segment of the population are sensitive to the toxins in the soda. Most people don't notice the negative effects for years.

Bill Clinton is a former President and has some of the best health care in the country and yet he has had two heart operations and never can remember anything. What did you always see Mr. Clinton pictured with? Diet Coke and McDonalds.

The National Soft Drink Association filed a protest letter prior to aspartame's approval stating that it was "uniquely unstable in aqeuous media" and the only studies showing aspartame safety were produced by the aspartame industry. One of the studies had a "placebo" of MSG so that the adverse reactions would not seem to differ.

The fact is not whether you feel sick after ingestion, it's that the levels of methanol, formaldehyde, formic acid and DKP DO exist in the sweetener, in increasing amounts when it sits around. This has been tested. The FDA does not care. It's your choice whether you ingest them.
 
I should of known you had an agenda.

You said you posted the same thing in a different topic and then this topic, then defended it again with another post.

So out of your 4 TOTAL posts on this board, 75% of them, that I know of, are geared towards bashing Diet Soda for the "supposed" negative effects.

When in truth there is not one study cited in the above ramblings, it's all wordy and theoretical. Yet there's no concrete studies or evidence. I don't even see anecdotal evidence, and even that, if there were any, and there isn't, doesn't have much merit to it.

BTW I'm referring to this

"What's wrong with aspartame?

Aspartame a.k.a. NutraSweet is a neurotoxic posion. It breaks down on the shelf or in the human body into several toxins and the amino acid d-phenylalanine. Those toxins being formaldehyde, methanol, formic acid and diketobenzaprine (DKP). Formaldehyde, boys and girls, is embalming fluid. Not too nice to the human body. Methanol is a wood alcohol which is present in aspartamein large amounts. In aspartame, it breaks down into formaldehyde and formic acid (fire ant venom). The FDA recommends a limit of 7.8 mg/day of methanol. A quart of aspartame-sweetened beverage contains about 56 mg methanol. DKP has been shown to cause brain cancer in lab rats. Furthermore, d-phenylalanine as present in aspartame is a free excitotoxin with similar effects to the amino in monosodium glutamate (d-glutamic acid). An excitotoxin is a chemical which can penetrate the brain barrier upon digestion in large amounts. When it reaches the brain, it causes overstimulation of the brain's neurons, so that they become very excited to the point of cell death. It's like forcing 100 watts of power through a 60 watt light bulb. Like little xmas lights on the brain, its neurons flicker faster and brighter until they burn out. Aspartame and MSG-like substances have been linked to major neurological disorders such as Multiple Sclerosis, Parkinson's Disease, Alzheimer's and Fibromyalgia, as well as numerous physical problems including macular degeneration, digestive issues and in an ironic twist, gross obesity. Some persons are more sensitive to feeling the effects of these substances than others, but they effect everyone to some degree as they are poisons, not allergens."

Where's the proof? Studies? Oh yea. There is none.

Before you jump on a bandwagon, atleast have some self respect for yourself, and make sure it has some proof in favor of it.
 
Oh and incase you didn't know, this is what a real scientific study looks like.

--------------------------------------

Aspartame: scientific evaluation in the postmarketing period.

Butchko HH, Stargel WW.

Medical and Scientific Affairs, The NutraSweet Company, Mt. Prospect, IL 60056, USA.

Prior to marketing, the safety of the high-intensity sweetener aspartame for its intended uses as a sweetener and flavor enhancer was demonstrated by the results of over 100 scientific studies in animals and humans. In the postmarketing period, the safety of aspartame was further evaluated through extensive monitoring of intake, postmarketing surveillance of anecdotal reports of alleged health effects, and additional research to evaluate these anecdotal reports and other scientific issues. The results of the extensive intake evaluation in the United States, which was done over an 8-year period, and the results of studies done in other countries demonstrated intakes which were well below the acceptable daily intakes set by the FDA and regulatory bodies in other countries, as well as the Joint FAO/WHO Expert Committee on Food Additives. Evaluation of the anecdotal reports of adverse health effects, the first such system for a food additive, revealed that the reported effects were generally mild and also common in the general population and that there was no consistent or unique pattern of symptoms that could be causally linked to consumption of aspartame. Finally, the results of the extensive scientific research done to evaluate these allegations did not show a causal relationship between aspartame and adverse effects. Thus, the weight of scientific evidence confirms that, even in amounts many times what people typically consume, aspartame is safe for its intended uses as a sweetener and flavor enhancer.

:welcome:
 
Whoa there. This happened to be a subject in two posts I was reading that I felt I could comment on, not to make up wild conspiracy theories. You can google anything I wrote and find all the evidence in the world should you like. I am happy to leave most subjects regarding supplements to the certainly more qualified experts on this board. However, this is something I have investigated very closely and I don't take it lightly. If you would like me to start posting links, I can do that. There are hundreds that I can post without looking far. We'll start with a few:

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I don't want to be disruptive on the board, so I'd like to end it there. You don't believe me, ok. But I'm not making this stuff up.
 
Oh and incase you didn't know, this is what a real scientific study looks like.

--------------------------------------

Aspartame: scientific evaluation in the postmarketing period.

Butchko HH, Stargel WW.

Medical and Scientific Affairs, The NutraSweet Company, Mt. Prospect, IL 60056, USA.
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Holy cow! I just read that.. you DO realize that study was done by the NUTRASWEET company, right?

Try this page instead:
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Fine, here's another one.
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Neuropsychological and biochemical investigations in heterozygotes for phenylketonuria during ingestion of high dose aspartame (a sweetener containing phenylalanine).

Trefz F, de Sonneville L, Matthis P, Benninger C, Lanz-Englert B, Bickel H.

Kreiskrankenhaus Reutlingen, Kinderklinik, Universitat Tubingen, Germany.

Aspartame, a high intensity sweetener, is used extensively worldwide in over 5,000 products. Upon ingestion, aspartame is completely metabolized to two amino acids and methanol (approximately 50% phenylalanine, 40% aspartic acid, and 10% methanol). The effects of aspartame on cognitive function, electroencephalograms (EEGs) and biochemical parameters were evaluated in 48 adult (21 men, 27 women) heterozygotes for phenylketonuria (PKUH), PKUH subjects whose carrier status had been proven by DNA analysis ingested aspartame (either 15 or 45 mg/kg/day) and placebo for 12 weeks on each treatment using a randomized, double-blind, placebo-controlled, crossover study. A computerized battery of neuropsychological tests was administered at baseline weeks -2 and -1, and during treatment at weeks 6, 12, 18, and 24. Samples for plasma amino acids and urinary organic acids were also collected during these visits. EEGs were evaluated by conventional and spectral analysis at baseline week -1 and treatment weeks 12 and 24. The results of the neuropsychological tests demonstrated that aspartame had no effect on cognitive function. Plasma phenylalanine significantly increased, within the normal range for PKUH, at 1 and 3 h following the morning dose of aspartame in the group receiving the 45 mg/kg per day dose only. There were no significant differences in the conventional or spectral EEG analyses, urinary organic acid concentrations, and adverse experiences when aspartame was compared with placebo. This study reaffirms the safety of aspartame in PKUH and refutes the speculation that aspartame affects cognitive performance, EEGs, and urinary organic acids.

Publication Types:
Clinical Trial
Randomized Controlled Trial

PMID: 8168806 [PubMed - indexed for MEDLINE]
-----------------------------

Is it just me, or every link I am clicking on that you have posted, I'm not seeing any actual long or even short term studies done to prove aspartame has negative effects in the human body.

I'm seeing a lot of people explain how they think aspartame theoretically works in the human body, but no concrete evidence of the actual effects of aspartame consumption.
 
Safety of long-term large doses of aspartame.

Leon AS, Hunninghake DB, Bell C, Rassin DK, Tephly TR.

Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis.

Safety of long-term administration of 75 mg/kg of aspartame per day was evaluated with the use of a randomized, double-blind, placebo-controlled, parallel-group design in 108 male and female volunteers aged 18 to 62 years. Subjects received either aspartame or placebo in capsule form three times daily for 24 weeks. No persistent changes over time were noted in either group in vital signs; body weight; results of standard laboratory tests; fasting blood levels of aspartame's constituent amino acids (aspartic acid and phenylalanine), other amino acids, and methanol; or blood formate levels and 24-hour urinary excretion of formate. There also were no statistically significant differences between groups in the number of subjects experiencing symptoms or in the number of symptoms per subject. These results further document the safety of the long-term consumption of aspartame at doses equivalent to the amount of aspartame in approximately 10 L of beverage per day.

Publication Types:
Clinical Trial
Randomized Controlled Trial

PMID: 2802896 [PubMed - indexed for MEDLINE]
 
Aspartame, proven insulin safe in even DIABETICS. If this doesn't even effect insulin in diabetics, how is it suppose to cause "gross obesity" again? Short answer, It doesn't.
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Aspartame use by persons with diabetes.

Nehrling JK, Kobe P, McLane MP, Olson RE, Kamath S, Horwitz DL.

Sixty-two subjects having either insulin-dependent or non-insulin-dependent diabetes completed a randomized, double-blind study comparing effects of aspartame or a placebo on blood glucose control. Twenty-nine subjects consumed 2.7 g aspartame per day for 18 wk, given as aspartame-containing capsules with meals, while 33 subjects took identical appearing placebo capsules. After 18 wk, no changes were seen in fasting or 2-h postprandial blood glucose levels or glycohemoglobin levels in either the aspartame- or placebo-treated groups. Adverse reactions were no more common in the group taking aspartame. We conclude that use of aspartame as a low-calorie sweetener does not adversely affect glycemic control of persons with diabetes.

Publication Types:
Clinical Trial
Randomized Controlled Trial

PMID: 3902420 [PubMed - indexed for MEDLINE]
 
Adverse Reactions to Aspartame:
Double-Blind Challenge in Patients from a Vulnerable Population

Biol. Psychiatry v.34 pp.13-17 1993

Ralph G. Walton, Robert Hudak, and Ruth J. Green-Waite

Department of Psychiatry, Northeastern Ohio Universities College of Medicine (RGW) and Department of Psychiatry (RGW) and Director of Research (RJG-W) Western Reserve Care System, Youngstown, OH; and Department of Psychiatry, University Hospitals of Cleveland, Cleveland, OH (RH).

Address reprint requests to Ralph G. Walton, MD, Department of Psychiatry, Western Reserve Care System, 500 Gypsy Lane, Youngstown, OH 44501.

Received October 3, 1992; revised March 31, 1993.

Abstract
This study was designed to ascertain whether individuals with mood disorders are particularly vulnerable to adverse effects of aspartame. Although the protocol required the recruitment of 40 patients with unipolar depression and a similar number of individuals without a psychiatric history, the project was halted by the Institutional Review Board after a total of 13 individuals had completed the study because of the severity of reactions within the group of patients with a history of depression.

In a crossover design, subjects received aspartame 30 mg/kg/day or placebo for 7 days. Despite the small n, there was a significant difference between aspartame and placebo in number and severity of symptoms for patients with a history of depression, whereas for individuals without such a history there was not. We conclude that individuals with mood disorders are particularly sensitive to this artificial sweetener and its use in this population should be discouraged.
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​
 
Woodrow C. Monte, Ph.D., R.D.
Director of the Food Science and Nutrition Laboratory
Arizona State University
Tempe, Arizona 85287

Published in Journal of Applied Nutrition, Volume 36, Number 1, 1984

 Abstract

 Aspartame (L-asparty-L-phenylalanine methyl ester), a new sweetener marketed under the trade name NutraSweet*, releases into the human bloodstream one molecule of methanol for each molecule of aspartame consumed.

This new methanol source is being added to foods that have considerably reduce caloric content and, thus, may be consumed in large amounts. Generally, none of these foods could be considered dietary methanol sources prior to addition of aspartame. When diet sodas and soft drinks, sweetened with aspartame, are used to replace fluid loss during exercise and physical exertion in hot climates, the intake of methanol can exceed 250 mg/day or 32 times the Environmental Protection Agency's recommended limit of consumption for this cumulative toxin(8).

There is extreme variation in the human response to acute methanol poisoning, the lowest recorded lethal oral dose being 100 mg/kg with one individual surviving a dose over ninety times this level (55). Humans, due perhaps to the loss of two enzymes during evolution, are more sensitive to methanol than any laboratory animal; even the monkey is not generally accepted as a suitable animal model (42). There are no human or mammalian studies to evaluate the possible mutagenic, teratogenic, or carcinogenic effects of chronic administration of methyl alcohol (55).

The average intake of methanol from natural sources varies but limited data suggests an average intake of considerably less than 10 mg/day (8). Alcoholics may average much more, with a potential range of between 0 and 600 mg/day, depending on the source and in some cases the quality of their beverages (15).

Ethanol, the classic antidote for methanol toxicity, is found in natural food sources of methanol at concentrations 5 to 500,000 times that of the toxin (Table 1). Ethanol inhibits metabolism of methanol and allows the body time for clearance of the toxin through the lungs and kidneys (40,46).

The question asked whether uncontrolled consumption of this new sweetener might increase the methanol intake of certain individuals to a point beyond which our limited knowledge of acute and chronic human methanol toxicity can be extrapolated to predict safety.
The consumption of aspartame sweetened soft drinks or other beverages in not limited by either calories or Osmolality, and can equal the daily water loss of an individual (which for active people in a state like Arizona can exceed 5 liters). The resultant daily methanol intake might then rise to unprecedented levels. Methanol is a cumulative toxin (8) and for some clinical manifestations it may be a human-specific toxin.
Conclusion

 Simply because methanol is found "naturally" in foods, we can not dismiss the need for carefully documented safety testing in appropriate animal models before allowing a dramatic increase in its consumption.

We know nothing of the mutagenic, teratogenic or carcinogenic effect of methyl alcohol on man or mammal (55,59). Yet, if predictions are correct (5) it won't be long before an additional 2,000,000 pound of it will be added to the food supply yearly (53).

Must this, then, constitute our test of its safety?

 *NutraSweet is a trademark of G.D. Searle & Co.
 
[font=Times New Roman,Times,Times NewRoman]FORMALDEHYDE DERIVED FROM DIETARY ASPARTAME BINDS TO TISSUE COMPONENTS IN VIVO

[/font][font=Times New Roman,Times,Times NewRoman]C. Trocho, R. Pardo, I. Rafecas, J. Virgili, X. Remesar, J.A. Ferná[/font]ndez-López and M. Alemany

[font=Times New Roman,Times,Times NewRoman]Departament de Bioquimica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, 08028 Barcelona Spain.

(Received in final form May 13, 1998)

Summary

Adult male rats were given an oral dose of 10 mg/kg aspartame [/font][font=Times New Roman,Times,Times NewRoman][size=-2]14[/size][/font][font=Times New Roman,Times,Times NewRoman]C-labelled in the methanol carbon. At timed intervals of up to 6 hours, the radioactivity in plasma and several organs was investigated. Most of the radioactivity found (>98 % in plasma, >75 % in liver) was bound to protein. Label present in liver, plasma and kidney was in the range of 1-2 % of total radioactivity administered per g or mL, changing little with time. Other organs (brown and white adipose tissues, muscle, brain, cornea and retina) contained levels of label in the range of 1/12 to 1/10th of that of liver. In all, the rat retained, 6 hours after administration about 5 % of the label, half of it in the liver. The specific radioactivity of tissue protein, RNA and DNA was quite uniform. The protein label was concentrated in amino acids, different from methionine, and largely coincident with the result of protein exposure to labelled formaldehyde. DNA radioactivity was essentially in a single different adduct base, different from the normal bases present in DNA. The nature of the tissue label accumulated was, thus, a direct consequence of formaldehyde binding to tissue structures. The administration of labelled aspartame to a group of cirrhotic rats resulted in comparable label retention by tissue components, which suggests that liver function (or its defect) has little effect on formaldehyde formation from aspartame and binding to biological components. The chronic treatment of a series of rats with 200 mg/kg of non-labelled aspartame during 10 days resulted in the accumulation of even more label when given the radioactive bolus, suggesting that the amount of formaldehyde adducts coming from aspartame in tissue proteins and nucleic acids may be cumulative. It is concluded that aspartame consumption may constitute a hazard because of its contribution to the formation of formaldehyde adducts.

Aspartame is one of the most widely used artificial sweeteners. Its peptide nature: aspartyl- phenylalanine methyl-ester facilitates its intestinal hydrolysis and the absorption (I -3) of innocuous amino acids together with small amounts of free methanol, far away from the lower limits of toxicity for that compound (4). The use of large amounts of aspartame in the diet, however, has been claimed to be the cause of a number of ailments, like headaches (5) and other symptoms (6-7), which are difficult to explain (8) from its known composition and the easy blending of its building components in the overall host metabolism. A number of studies have linked aspartame with neurologic pathologies, but most of the results yielded negative or inconclusive correlations (9-16). The acute toxicity of aspartame is believed to be low (I7), which has promoted a wide distribution of the product as a potent hypocaloric and safe substitute of sugar (I 8-19).

Methanol is primarily oxidized in several tissues to formaldehyde and formic acid (20-2 1), the latter being considered the main metabolite responsible for the deleterious effects of acute methanol intoxication in man (22), but also in experimental animals (23), in spite of the marked resistance of the rat to formate (24-25). The enzymes involved in methanol metabolism are alcohol dehydrogenase (EC 1. 1. 1. 1) and aldehyde dehydrogenase (EC 1.2.1.3), as well as the microsomal oxidase pathway (26). Acute methanol intoxication may produce blindness and hepatic loss of function (27-28), since the retina, cornea and liver contain the highest alcohol dehydrogenase activity (29-30). These tissues are, thus, where one can expect, eventually, the largest accumulation of their byproducts: formaldehyde and formate, in the event of intoxication. It may be assumed that liver functional failure due to cirrhosis could result in the loss of its role as barrier to intestinal methanol, and thus, the effects of methanol intoxication on other tissues (i.e. the retina) would be more marked. The cirrhotic rat may be, then, used as a model of acute or chronic methanol toxicity.

Formaldehyde is a highly reactive small molecule which strongly binds to proteins (3 1) and nucleic acids (32) forming adducts which are difficult to eliminate through the normal metabolism pathways.

As a result, formaldehyde induces severe functional alterations (33), including the development of cancer (34). The small amounts of formaldehyde which can be potentially produced from dietary use of aspartame have been often overlooked in its potential toxicity precisely because of the limited amount eventually produced. However, the administration of labelled aspartame to experimental animals results in the incorporation of a significant proportion of the label to proteins (35). The accumulation of label has been postulated to be the consequence of label drift into amino acids (essentially in the methionine methyl group) through the one-carbon pool (35). This aspect has not been, however, proved nor further investigated.

We have intended here to determine the extent of conversion of aspartame methanol to formaldehyde and its eventual effect on the overall physiologic function of the rat. In addition we have probed whether the aspartame methanol carbon presence in tissue components is due to the eventual drift of label into methionine and nucleic acid components through the one-carbon pool, or is the consequence of a direct reaction with free formaldehyde forming stable adducts.
[font=Times New Roman,Times,Times NewRoman][size=+1]Discussion
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[/size][/font][font=Times New Roman,Times,Times NewRoman][/font][font=Times New Roman,Times,Times NewRoman]The lower incorporation of methanol label in most tissues of cirrhotic rats, compared with controls, may be the consequence of reduced liver uptake of substrates, but also the result of a reduced overall metabolic activity in the damaged liver of the rats (44). These effects are clearly reflected by their stunted growth and high mortality rate during the intoxication process, of about 50 % of the rats (36). The relative insignificance of the differences between the normal and cirrhotic groups indicates that the liver is not essential in the process of transfer of aspartame carbon to tissue proteins, i.e. that there is not a direct relationship between the ability to process alcohols and the retention of methanol carbon, bound to tissue components.

The high label presence in plasma and liver is in agreement with the carriage of the label from the intestine to the liver via the portal vein. The high label levels in kidney and, to a minor extent, in brown adipose tissue and brain are probably a consequence of their high blood flows (45). Even in white adipose tissue, the levels of radioactivity found 6 hours after oral administration were 1/25th those of liver. Cornea and retina, both tissues known to metabolize actively methanol (21,28) showed low levels of retained label. In any case, the binding of methanol-derived carbon to tissue proteins was widespread, affecting all systems, fully reaching even sensitive targets such as the brain and retina.

In all groups studied, the label bound found in plasma and tissues corresponds to that injected with aspartame, since there is no other source of radioactivity available. The lack of changes in plasma radioactivity from 1 to 24 h suggests that the half life of this newly added carbon was quite long, thus precluding the possibility that the label detected would simply correspond to unattached methanol. The label bound to plasma proteins was not aspartame either, since the latter is a non-reactive molecular species fully hydrolysed in the intestine (1-2); the peptide never arrived to be in contact with the rat tissues or its components. We were not able to reproduce any direct labelling of protein exposed either to aspartame, methanol nor formic acid.

Most of the label found in the tissues is the result of the formation of formaldehyde or (in smaller proportion in any case, because of its lower reactivity) formate adducts. Methanol is highly volatile and, eventually, its radioactivity could hardly be taken into account, since the counting method already eliminates this possibility. In addition, the stabilized maintenance of the plasma radioactivity levels could not belong to formate nor methanol, since these unattached substrates are easily taken up and oxidized by tissues, filtered by the kidney or even lost through respiration as occurs with short chain volatile alcohols. The shape of the time-course graph representing the changes in tissue label supports the hypothesis assuming that the label is firmly bound at least for 6 hours after administration of aspartame. This behaviour is also found in formaldehyde-protein adducts (3 1), long lived species difficult to eliminate, in which the protein is denatured and its original function altered.

The transfer of "one-carbon" units from aspartame to plasma and tissue proteins has been known for a time (35). Its nature, and the mechanism of attachment, however, were assumed to be due to the incorporation of the methanol carbon to normal amino acid structures (essentially forming the methyl group of methionine) through the "one-carbon " tetrahydrofolate and S-adenosyl-rnethionine pathways (35). The lack of radioactivity in the methionine spot from aspartme-treated labelled rat proteins, however, shows that this assumption could no longer be maintained. The finding of other -different- labelled DNP-derivatized amino acid(s) in the exposed protein hydrolysates confirms that the label was not carried into protein through the one-carbon pool metabolism labelling of methionine, i.e. prior to the synthesis of the protein. The coincidence of this labelled DNP-amino acid residue with that obtained from protein experimentally exposed to formaldehyde confirms that the label fixed to rat proteins after labelled aspartame exposure was derived from formaldehyde adducts, and definitely proves that the label in tissue proteins does not correspond to methionine.

This agrees with the incorporation of the label into the fully synthesized protein at a remarkably uniform rate of label distribution between different molecular species in spite of their eventually different turnover (synthesis) rates.

The analysis of label distribution in the nucleic acids shows a remarkable uniformity in the specific activities of DNA and protein, with RNA showing somewhat lower values in the same range. This distribution is in agreement with a fairly uniform exposure to the same reacting species, and could not be explained through incorporation of one-carbon pathways into molecules which show widely different half lives, as is the case with the highly recycled RNA and some proteins and long-lived DNA and proteins. The finding of large amounts of label in DNA, higher than in RNA, could be only explained through direct reaction, since its slow turnover would require inordinately long exposure times to achieve the observed specific activities. The additional existence of different labelled bases, probably formed by the binding of formaldehyde and the "normal" bases not coinciding with any of the other bases. The thin layer chromatograius show a single spot, resolved in at least three peaks, none of which coincided with adenine, guanine nor thymine. The lack of label in these spots is incompatible with the "one-carbon" pathways hypothesis of label incorporation, since two "IC" units are needed for the synthesis of adenine and guanine and one for that of thymine. The presence of label in other different molecules strongly supports the adduct formation postulate, attributing to formaldehyde the main responsibility for the appearance of aspartame- methanol label in tissue components. The evidence presented, then, proves that a significant portion of the methanol carbon of aspartame finds its way into adducts of proteins and nucleic acids under the conditions tested, both in normal and cirrhotic rats. The results presented show that the carbon adducts of protein and DNA could have been generated only from formaldehyde derived from aspartame methanol, since all the otherbiochemical forms in which this carbon may be found could not produce adducts with protein and nucleic acids.

The doses of aspartame given to the rats in this experiment were high, higher at least than that any human may receive daily with normal consumption of the additive -in the range of 2-6 mg/kg-day (46)-, but were similar to those used in comparable tests on rodents in which no ill-effects were detected. These doses were in the same range as the adi for humans established for Canada and the EC (40 mg/kg-day) (46). The dose administered was also lower than that used for toxicity studies, which have shown that even at very high doses aspartame does not produce immediately appreciable harm (I 7). Most of these studies, however, refer to direct acute toxicity effects, which were not observed either in the rats used in the present study (except, perhaps, for softer droppings in those subjected to the chronic treatment with aspartame gavages).

The amount of label recovered in tissue components was quite high in all the groups, but especially in the NA rats. In them, the liver alone retained, for a long time, more than 2 % of the methanol carbon given in a single oral dose of aspartame, and the rest of the body stored an additional 2 % or more. These are indeed extremely high levels for adducts of formaldehyde, a substance responsible of chronic deleterious effects (33) that has also been considered carcinogenic (34,47). The repeated occurrence of claims that aspartame produces headache and other neurological and psychological secondary effects -more often than not challenged by careful analysis- (5,9,10,15,48) may eventually find at least a partial explanation in the permanence of the formaldehyde label, since formaldehyde intoxication can induce similar effects (49).

The cumulative effects derived from the incorporation of label in the chronic administration model suggests that regular intake of aspartame may result in the progressive accumulation of formaldehyde adducts. It may be further speculated that the formation of adducts can help to explain the chronic effects aspartame consumption may induce on sensitive tissues such as brain (6,9,19,50). In any case, the possible negative effects that the accumulation of formaldehyde adducts can induce is, obviously, long-term. The alteration of protein integrity and function may needs some time to induce substantial effects. The damage to nucleic acids, mainly to DNA may eventually induce cell death and/or mutations. The results presented suggest that the conversion of aspartame methanol into formaldehyde adducts in significant amounts in vivo should to be taken into account because of the widespread utilization of this sweetener. Further epidemiological and long-term studies are needed to determine the extent of the hazard that aspartame consumption poses for humans.

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Alright I guess since there are conflicting studies, it is up to the consumers decide.

All I can say is, with my main study there was 108 male and female volunteers between the ages of 18-62, who comsumed 75mg/kg (A SHITLOAD) of aspartame a day for 24 full weeks and experienced nothing different than the placebo group.

and there's Brooklyn's study where 40 patients with unipolar depression and a similiar number of patients without a history of depression. The project being halted because the patients with unipolar depression, couldn't handle the aspartame. Not the normal patients, I just want to add. The ones with unipolar depression.

"We conclude that individuals with mood disorders are particularly sensitive to this artificial sweetener and its use in this population should be discouraged."

Oh man... I could have a field day with this conclusion. First and last of all, it wasn't mood disorders, it was unipolar depression. I gaurentee on the average day these folks are so unstable you could do a study on them with WATER consumption and they would freak out.
 
Neurology. 1992 May;42(5):1000-3

Aspartame exacerbates EEG spike-wave discharge in children with generalized absence epilepsy: a double-blind controlled study.

Camfield PR, Camfield CS, Dooley JM, Gordon K, Jollymore S, Weaver DF.

IWK Children's Hospital, Halifax, Nova Scotia, Canada.

There are anecdotal reports of increased seizures in humans after ingestion of aspartame. We studied 10 children with newly diagnosed but untreated generalized absence seizures. Ambulatory cassette recording of EEG allowed quantification of numbers and length of spike-wave discharges in a double-blind study on two consecutive days. On one day the children received 40 mg/kg aspartame and on the other day, a sucrose-sweetened drink. Baseline EEG was the same before aspartame and sucrose. Following aspartame compared with sucrose, the number of spike-wave discharges per hour and mean length of spike-wave discharges increased but not to a statistically significant degree. However, the total duration of spike-wave discharge per hour was significantly increased after aspartame (p = 0.028), with a 40% +/- 17% (SEM) increase in the number of seconds per hour of EEG recording that the children spent in spike-wave discharge. Aspartame appears to exacerbate the amount of EEG spike wave in children with absence seizures. Further studies are needed to establish if this effect occurs at lower doses and in other seizure types.
 
Got any studies on normal people?

Somehow I doubt the average aspartame diet soda drinker, has unipolar depression or is a child with generalized absence epilepsy. Call it a hunch...
 
All I can say is, with my main study there was 108 male and female volunteers between the ages of 18-62, who comsumed 75mg/kg (A SHITLOAD) of aspartame a day for 24 full weeks and experienced nothing different than the placebo group.
Click to expand...
This study you quote was, again, sponsored by Searle, the NutraSweet company. Quoting only studies funded by the aspartame company would be like me releasing a "miracle cancer drug" and saying, "Sure it works. I checked it myself."
 
Safety of long-term large doses of aspartame.

Leon AS, Hunninghake DB, Bell C, Rassin DK, Tephly TR.

Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis.

Where does that say Searle? wait... It doesn't. :cheers:
 
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