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| | #31 |
| Gate Keeper Board Moderator | Pop? what is this 1950. 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. ![]() |
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| | #32 | |||
| Gold Member | Quote:
On a more serious note, the question was asked about diet soda. I posted this earlier in another thread: Quote:
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| | #33 |
| Registered User | 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. |
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| | #34 | |
| Gold Member | Quote:
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. | |
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| | #35 |
| Registered User | 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. |
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| | #36 |
| Registered User | 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. ![]() |
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| | #37 | |
| Registered User | Quote:
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| | #38 |
| Gold Member | 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: http://www.321recipes.com/aspartame.html http://www.dorway.com/ http://www.newmediaexplorer.org/chri..._poisoning.htm 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. |
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| | #39 | |
| Gold Member | Quote:
Try this page instead: http://www.dorway.com/peerrev.html | |
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| | #40 |
| Registered User | Fine, here's another one. ------------------------------------------ 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. |
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| | #41 |
| Registered User | 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] |
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| | #42 |
| Registered User | 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. -------------------------------------- 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] |
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| | #43 |
| Gold Member | 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 |
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| | #44 |
| Gold Member | 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. |
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| | #45 |
| Gold Member | FORMALDEHYDE DERIVED FROM DIETARY ASPARTAME BINDS TO TISSUE COMPONENTS IN VIVO C. Trocho, R. Pardo, I. Rafecas, J. Virgili, X. Remesar, J.A. Fernández-López and M. Alemany 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 14C-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. Discussion 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 o |