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  1. #1
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    Post Artifical Sweeteners: An Overview

    Artificial Sweeteners: An Overview
    by pogue

    Artificial Sweeteners have become a common topic of interest and discussion. Some individuals are very concerned about the safety of these sweeteners, because they are "unnatural chemicals". When the term unnatural, artificial and chemical is applied to something, it can make it sound scary. However, artificial sweeteners are typically much safer overall than plain sucrose or high fructose corn syrup. Both sucrose and HFCS cause large spikes of insulin, which can lead to insulin sensitivity, fat storage and increased hunger with carb cravings. Although, these have their place in an athletes regime, being most useful in the window before, during and after a workout whereby an insulin spike will have a positive effect on restoring glucose to muscles, and increasing skeletal protein stores. Using these sweeteners, despite the fact that they are natural, have a potential to cause more overall health ailments in the long term than any artificial sweetener. Sweeteners with a high glycemic index have been implicated in increased risk for obesity and diabetes, amongst other problems.

    For individuals who lead a healthy life style, be it low carb, low fat, or even looking for increased overall mass can all benefit from the use of artifical sweetners everyday. When in doubt, always pick Diet soda over regular soda, and sweeten your coffee with the pink or blue packets, instead of white or brown. You'll be glad you did.

    Artificial Sweeteners - Debunking The Myths!


    Why is this thread closed?

    This thread was originally written as an informative article to help those who have been flooded with misinformation about artificial sweeteners and their supposed ill-effects on the body. Performing a simple search on any of the major search engines for any of the artificial sweeteners listed below turns up all sorts of conspiracy theorist pages as the first results. Unfortunately, because of this and the large amount of other misinformation out there posted by individuals who have no scientific understanding, many people automatically assume that the assertions made by these groups & people are true. This has caused great animosity towards anyone who tries to discuss the facts of these compounds and have a real discussion on them in a scientific nature. Anyone who appears to be trying to "defend" ingredients such as aspartame causes a large number of people, who seemingly come out of the woodwork, to post a wide range of unreasonable assertions that cannot be proved or disproved, and thus there is no way to draw any conclusions from them. Yet, because the people who post these messages use those arguments as the core of their belief, it is impossible to even try and get them to look at them more rationally and makes any further discussion of the topic completely pointless -- it's essentially akin to a child sticking their fingers in their ears and singing loudly to try and ignore any sort of reasonable debate or alternate opinion you might try and show them. That makes it quite unfortunate for anyone who has a reasonable question about these ingredients, because others have ruined it for them. It's because of the constant barrage of these kinds of post in this article that it has been closed. Since I have posted this, other threads have been started on this same discussion that include a great deal of knowledge from other board members, included our resident biochemist Layne Norton (str8flexed), which I recommend anyone who is interested in the topic read through and is welcome to continue the discussion there.

    ACSH artificial sweetener report updated.

    The American Council on Science and Health has revised its report on acesulfame-K, aspartame, neotame, saccharin, sucralose, and three other artificial sweeteners that are approved for use in other countries. The report states that these products may enable people to improve their diet by getting calories from more nutritious foods rather than from sugar in soft drinks. It notes, however, that whether sugar substitutes help people lose weight is not scientifically settled. Sugar alcohols are also discussed. The report, Sugar Substitutes and Your Health, can be ordered in booklet form for $5 or can be read online at http://www.acsh.org/publications/pub...pub_detail.asp
    The document is attached as a PDF.
    Attached Files

  2. #2
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    Post Aspartame (Nutrasweet)

    Aspartame

    Aspartame, brand name Nutrasweet, has been an artificial sweetener in wide use since 1981. It is a derivative of the essential amino acid, phenylalanine, which is commonly found in most protein sources. It was discovered on accident when a chemist combined phenylalanine with aspartic acid (another amino acid), tasted it and determined it was sweet. Aspartame is 160 times sweetener than sucrose, and is commonly found in diet soft drinks and numerous food products. It has no calories, carbs, protein or fat and does not spike insulin levels, as sucrose does - making it safe for diabetic consumption. The only issue with aspartame is with individuals who have a disorder known as "phenylketonuria", which is what the cryptic warning on soda cans refers to.

    There are numerous sites on the internet claiming that aspartame is dangerous and can cause a wide variety of ailments. Everything ranging from heart attacks, brain tumors, cancer, and death is attributed to aspartame, with absolutely no medical data to prove it. There is a ton of misinformation on this chemical. For no good reason, it has been demonized by some individuals who seem to have a vendetta against the medical community, the government or chemical companies. I guess someone forgot to tell them about all the antifreeze in their shampoo. Still, despite overwhelming evidence to the contrary, these people refuse to believe that aspartame is safe. You'd have a hard time convincing me that two amino acids that are found in everyones diet are dangerous when combined, which is a major fault in the logic of their argument. Yet, the myths still persist.

    The truth is aspartame is one of the most clinically studied chemicals in the world, with an overall excellent safety profile. The ADI (acceptable daily intake) for aspartame is 40mg/kg.

    Here are some reads on the topic:
    Aspartame Info from Wikipedia
    Aspartame History & Synthesis w/ molecular diagrams
    Aspartame Myths Debunking from Snopes
    Aspartame Info from the FDA
    Calorie Control info on Aspartame
    Aspartame Safety Review by Paul Cribb from AST

    Now on to the studies. Note that these are the most recent studies on the subject. The first two are by Nutrasweet, which some may claim as being bias. However, keep in mind that these are peer reviewed medical studies and there are many more where this came from for individuals who want to take the time to research the facts.
    Aspartame: review of safety.

    Butchko HH, Stargel WW, Comer CP, Mayhew DA, Benninger C, Blackburn GL, de Sonneville LM, Geha RS, Hertelendy Z, Koestner A, Leon AS, Liepa GU, McMartin KE, Mendenhall CL, Munro IC, Novotny EJ, Renwick AG, Schiffman SS, Schomer DL, Shaywitz BA, Spiers PA, Tephly TR, Thomas JA, Trefz FK.

    Medical and Scientific Affairs, The NutraSweet Company, Mt Prospect, Illinois 60056, USA. harriett.h.butchko@nutrasweet.com

    Over 20 years have elapsed since aspartame was approved by regulatory agencies as a sweetener and flavor enhancer. The safety of aspartame and its metabolic constituents was established through extensive toxicology studies in laboratory animals, using much greater doses than people could possibly consume. Its safety was further confirmed through studies in several human subpopulations, including healthy infants, children, adolescents, and adults; obese individuals; diabetics; lactating women; and individuals heterozygous (PKUH) for the genetic disease phenylketonuria (PKU) who have a decreased ability to metabolize the essential amino acid, phenylalanine. Several scientific issues continued to be raised after approval, largely as a concern for theoretical toxicity from its metabolic components--the amino acids, aspartate and phenylalanine, and methanol--even though dietary exposure to these components is much greater than from aspartame. Nonetheless, additional research, including evaluations of possible associations between aspartame and headaches, seizures, behavior, cognition, and mood as well as allergic-type reactions and use by potentially sensitive subpopulations, has continued after approval. These findings are reviewed here. The safety testing of aspartame has gone well beyond that required to evaluate the safety of a food additive. When all the research on aspartame, including evaluations in both the premarketing and postmarketing periods, is examined as a whole, it is clear that aspartame is safe, and there are no unresolved questions regarding its safety under conditions of intended use.
    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.
    Aspartame: neuropsychologic and neurophysiologic evaluation of acute and chronic effects.

    Spiers PA, Sabounjian L, Reiner A, Myers DK, Wurtman J, Schomer DL.

    Clinical Research Center, Massachusetts Institute of Technology, Cambridge 02139, USA.

    BACKGROUND: Neurobehavioral symptoms have been reported anecdotally with aspartame. OBJECTIVE: This study sought to determine whether aspartame can disrupt cognitive, neurophysiologic, or behavioral functioning in normal individuals. DESIGN: Forty-eight healthy volunteers completed a randomized, double-blind, placebo-controlled, crossover study. The first month was aspartame free. Subjects then consumed sodas and capsules with placebo, aspartame, or sucrose for 20 d each. Order was randomized and subjects were assigned to either a high- (45 mg x kg body wt(-1) x d(-1)) or low- (15 mg x kg body wt(-1) x d(-1)) dose aspartame group. Neuropsychologic and laboratory testing was done on day 10 of each treatment period to determine possible acute effects and on day 20 for possible chronic effects. RESULTS: Plasma phenylalanine concentrations increased significantly during aspartame treatment. Neuropsychologic results; adverse experiences; amino acid, insulin, and glucose values; and electroencephalograms were compared by sex and by treatment. No significant differences were found for any dependent measure. CONCLUSION: Large daily doses of aspartame had no effect on neuropsychologic, neurophysiologic, or behavioral functioning in healthy young adults.
    Last edited by pogue; 11-11-2006 at 06:10 AM.
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    Post Sucralose (Splenda)

    Sucralose

    Sucralose, brand name Splenda, is a relatively new artificial sweetener on the market. Like, aspartame, it has no calories, carbs, fat or protein and does not adversly effect insulin levels. "It is manufactured by chlorinating sugar, which substitutes three chlorine atoms for three hydroxyl groups to produce 4,1',6'-trichlorogalacto-sucrose".
    --Wikipedia

    Sucralose has made it's way into a variety of food products, including soft drinks, ice cream, and candy bars. It is 600 times sweeter than sucrose. Sucralose simply passes throughout the body, and is not processed - merely consumed and secreted. The brand name Splenda uses a combination of sucralose and maltodextrin, which gives it 2 calories per packet. Sucralose is suitable for all people, including diabetics. The ADI of sucralose is 15mg/kg.

    Sucralose is one of the safest artificial sweeteners available. It is my personal choice of sweetener, because it tastes closest to real sugar and can be used in just about anything. Diet Rite soda uses a combination of sucralose and acesulfame to sweeten it, so it would be a good choice for people who want to avoid aspartame. I didn't like the taste myself though, and prefer Diet Coke or Pepsi.
    Wikipedia article on Sucralose
    Calorie Counter Info on Sucralose

    The studies:

    Repeated dose study of sucralose tolerance in human subjects.

    Baird IM, Shephard NW, Merritt RJ, Hildick-Smith G.

    Pine Court, Fairbourne, Cobham, Surrey KT11 2BT, UK.

    Two tolerance studies were conducted in healthy human adult volunteers. The first study was an ascending dose study conducted in eight subjects, in which sucralose was administered at doses of 1, 2. 5, 5 and 10mg/kg at 48-hour intervals and followed by daily dosing at 2mg/kg for 3 days and 5mg/kg for 4 days. In the second study, subjects consumed either sucralose (n=77) or fructose (50g/day) (n=31) twice daily in single blind fashion. Sucralose dosage levels were 125mg/day for weeks 1-3, 250mg/day during weeks 4-7, and 500mg/day during weeks 8-12. No adverse experiences or clinically detectable effects were attributable to sucralose in either study. Similarly, haematology, serum biochemistry, urinalysis and EKG tracings were unaffected by sucralose administration. In the 13-week study, serial slit lamp ophthalmologic examination performed in a random subset of the study groups revealed no changes. Fasting and 2-hour post-dosing blood sucralose concentrations obtained daily during week 12 of the study revealed no rising trend for blood sucralose. Sucralose was well tolerated by human volunteers in single doses up to 10mg/kg/day and repeated doses increasing to 5mg/kg/day for 13 weeks. Based on these studies and the extensive animal safety database, there is no indication that adverse effects on human health would occur from frequent or long-term exposure to sucralose at the maximum anticipated levels of intake.
    Sucralose metabolism and pharmacokinetics in man.

    Roberts A, Renwick AG, Sims J, Snodin DJ.

    University of Southampton, Bassett Crescent East, Southampton SO9 3TU, UK.

    The metabolic and pharmacokinetic profile of sucralose was studied in human volunteers. Following a single oral dose of (14)C-sucralose (1mg/kg, 100 microCi) to eight male subjects, a mean of 14.5% (range 8.9 to 21.8%) of the radioactivity was excreted in urine and 78.3% (range 69.4 to 89.6%) in the faeces, within 5 days. The total recovery of radioactivity averaged 92.8%. Plasma concentrations of radioactivity were maximal at about 2 hours after dosing. The mean residence time (MRT) for sucralose was 18.8hr, while the effective half-life for the decline of plasma radioactivity was 13hr. Two volunteers given a higher oral dose (10mg/kg, 22.7 microCi) excreted a mean of 11.2% (9.6 and 12.7%) of the radioactivity in urine, and 85.5% (84.1 and 86.8%) in faeces over 5 days. The total recovery of radioactivity was 96.7%. The radiolabelled material present in faeces was essentially unchanged sucralose. Sucralose was the principal component in the urine together with two more polar components which accounted for only 2.6% of the administered dose (range 1.5 to 5.1% of dose); both metabolites possessed characteristics of glucuronide conjugates of sucralose.
    Glycemic effect of a single high oral dose of the novel sweetener sucralose in patients with diabetes.

    Mezitis NH, Maggio CA, Koch P, Quddoos A, Allison DB, Pi-Sunyer FX.

    Division of Endocrinology, Diabetes and Nutrition, St. Luke's-Roosevelt Hospital Center, New York, NY 10025, USA. nhm2@columbia.edu

    OBJECTIVE: To examine the effect of a single high oral dose of the novel noncaloric sweetener sucralose on short-term glucose homeostasis in patients with IDDM or NIDDM. RESEARCH DESIGN AND METHODS: A total of 13 IDDM and 13 NIDDM patients with glycosylated hemoglobin levels < 10% completed this double-blind cross-over study. After an overnight fast, patients were administered opaque capsules containing either 1,000 mg sucralose or cellulose placebo, followed by a standardized 360-kcal liquid breakfast. Plasma glucose and serum C-peptide levels were measured over the next 4 h. RESULTS: Regardless of the type of diabetes, areas under the curves for changes of plasma glucose and serum C-peptide levels after sucralose administration were not significantly different from those after placebo. During test meals with sucralose, one episode of symptomatic hypoglycemia occurred in each of three IDDM patients, but these episodes were not considered the result of sucralose administration. CONCLUSIONS: The present results support the conclusion that sucralose consumption does not adversely affect short-term blood glucose control in patients with diabetes.
    Last edited by pogue; 11-11-2006 at 06:11 AM.
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  4. #4
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    Post Sucralose (Continued)

    Sucralose (Continued)

    Acute and subchronic toxicity of sucralose.

    Goldsmith LA.

    McNeil Specialty Products Company, 501 George St, New Brunswick, NJ 08903, USA.

    The toxicity of sucralose has been evaluated in acute and subchronic toxicity studies. Acute oral toxicity studies in male and female mice and male rats documented no deaths or treatment-related signs at doses of 16g/kg for mice and 10g/kg for rats. Sucralose was administered to male and female rats for 4 and 8 weeks at dietary concentrations of 1.0, 2.5 or 5.0%. Achieved dose ranges (mg/kg/day) for the respective dietary levels were 737-1287, 1865-3218 and 2794-6406. There were no toxicologically significant effects observed at the 1.0% or 2.5% dietary levels. However, decreases in food consumption, body weight gain and selected organ weights and ratios as well as splenic and thymic histopathologic changes occurred in rats administered 5.0% for 4 or 8 weeks. A gavage study wherein doses of 0, 750, 1500 or 3000mg/kg/day were administered to male and female rats for 26 weeks investigated further the observations from the dietary study as well as general subchronic toxicity. The gavage study documented no sucralose-related toxicity. These results implicate the reduced palatability and digestibility of diets containing high concentrations of sucralose seen in the diet study as the cause for the decreased food consumption and other accompanying alterations. Dose selection for chronic toxicity studies in rats took into consideration the effect of high concentrations of sucralose on digestion and food consumption and the limitations that would be imposed on subsequent studies. In male and female dogs, no sucralose-related adverse effects were observed following the dietary administration of 0.3, 1.0 or 3.0% for 12 months achieving doses of approximately 90, 300 and 900mg/kg/day respectively. These studies establish that sucralose is non-toxic in rodents following acute oral administration. The rat no-observed-adverse-effect level ranged between 2.5 and 5.0% following subchronic dietary administration. A 3.0% dietary concentration equivalent to a dose of 900mg/kg/day produced no adverse effects in beagle dogs when fed for 12 months.
    That would mean that 150lb human would need to consume 612g of sucralose a day to have adverse effects.

    Effect of sucralose in coffee on plaque pH in human subjects.

    Steinberg LM, Odusola F, Mandel ID.

    Center for Clinical Research, Columbia University, School of Dental and Oral Surgery, New York, N.Y., USA.

    Our earlier work demonstrated that the sweetener sucralose, C12 H19 CI3 O8, mixed with water had no effect on intraoral plaque pH. The current study compared the effect on resting plaque pH of sucralose to sucrose when these sweeteners were used in hot coffee at equivalent sweetness levels. Twelve subjects with an identified acidogenic plaque were tested at dicrete sessions, using coffee as vehicle with: (1) sucrose; (2) sucralose; (3) sucralose plus maltodextrin (SM); (4) sucralose plus dextrose and maltodextrin (SMD), and (5) no additional sweetener. Each subject rinsed for 1 min with the test rinse, expectorated, and plaque pH was measured at six dental sites for 60 min using an antimony touch electrode method. Data were summarized for baseline pH, delta pH (baseline pH minus lowest pH attained), minimum pH, and area under the pH curve (AUC). Baseline pH was not different throughout all tests. Quantification of AUC in the various groups showed that sucralose with coffee had no statistically significant impact on plaque acidogenesis. AUC, minimum pH and delta pH were least changed by coffee and sucralose, while the SM and SMD combinations generally led to intermediate changes as compared with coffee sweetened with sucrose or sucralose. Because of its acidic nature, unsweetened coffee led to a modest pH depression, the effect of which appears to be blunted by sucralose. This study confirms that sucralose is non-acidogenic and indicates that sucralose may reduce the acidogenic potential of coffee.
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    Post Stevia

    Stevia

    Stevia, or steviosides, is a plant derived sweetener which is becoming more commonly used in food and beverage products. In the US, stevia can only be sold as a dietary supplement in food additives, and not as a sweetener since it is not approved for that usage. The FDA has gone so far as to order recalls from some manufacturers who had stevia listed as a sweetener on containers of protein powder. This is due to the fact that there has been some concerns with animal studies and fertility in stevia. However, there is a lacking of evidence in humans to support this conclusions. There is very little evidence on safety and toxicology on steviosides in humans. Since you can't patent a natural substance in US, there is little motive for companies to fund studies on it. Other manufacturers could market stevia using the same data, and no residuals would be paid to the company who funded the study. This puts stevia in sweetener limbo.

    In animal studies, we see that stevia can cause some issues with fertility, carbohydrate metabolism, and possibly converting to a carcinogen in vitro.

    Stevia is a plant that generally grows in South America and is approved in Japan as a sweetener. It is 200-300 times sweetener than sucrose and does not have an effect on insulin levels. The ADI of stevia is 7.9mg/kg. I could not find any data to determine the calorie amount typically found in stevia, but I would assume that is little to none.

    Stevia Article from Wikipedia
    Stevioside from Calorie Control
    Stevia Review from CSPI

    Here are some studies. As mentioned, there are little to no studies done in vivo on humans. Take that into consideration when using stevia in large amounts.
    Measurement of the relative sweetness of stevia extract, aspartame and cyclamate/saccharin blend as compared to sucrose at different concentrations.

    Cardello HM, Da Silva MA, Damasio MH.

    Department of Food and Nutrition, FCF-UNESP, Araraquara, SP, Brazil. cardhel@fcfar.unesp.br

    Special diets are used to mitigate many human diseases. When these diets require changes in carbohydrate content, then sweetness becomes an important characteristic. The range of low-calorie sweeteners available to the food industry is expanding. It is essential to have an exact knowledge of the relative sweetness of various sweeteners in relation to different sucrose concentrations. The objective of this study was to determine the variation on the relative sweetness of aspartame (APM), stevia [Stevia rebaudiana (Bert.) Bertoni] leaf extract (SrB) and the mixture cyclamate/saccharin--two parts of cyclamate and one part of saccharin--(C/S) with the increase in their concentrations, and in neutral and acid pH in equisweet concentration to 10% sucrose, using magnitude estimation. Sweetness equivalence of SrB in relation to sucrose concentrations of 20% or higher and of APM and C/S to sucrose concentrations of 40% or higher could not be determined, because a bitter taste predominated. The potency of all sweeteners decreased as the level of sweetner increased. In equi-sweet concentration of sucrose at 10%, with pH 7.0 and pH 3.0, the potency was practically the same for all sweeteners evaluated.
    Efficacy and tolerability of oral stevioside in patients with mild essential hypertension: a two-year, randomized, placebo-controlled study.

    Hsieh MH, Chan P, Sue YM, Liu JC, Liang TH, Huang TY, Tomlinson B, Chow MS, Kao PF, Chen YJ.

    Department of Medicine, Taipei Medical University--Wan Fang Hospital, Taipei City, Taiwan.

    BACKGROUND: Stevioside, a natural glycoside isolated from the plant Stevia rebaudiana Bertoni, has been used as a commercial sweetening agent in Japan and Brazil for >20 years. Previous animal and human studies have indicated that stevioside has an antihypertensive effect. OBJECTIVES: This study was undertaken to investigate the long-term (2-year) efficacy and tolerability of stevioside in patients with mild essential hypertension. Secondary objectives were to determine the effects of stevioside on left ventricular mass index (LVMI) and quality of life (QOL). METHODS: This was a multicenter, randomized, double-blind, placebo-controlled trial in Chinese men and women aged between 20 and 75 years with mild essential hypertension (systolic blood pressure [SBP] 140-159 mm Hg and diastolic blood pressure [DBP] 90-99 mm Hg). Patients took capsules containing 500 mg stevioside powder or placebo 3 times daily for 2 years. Blood pressure was measured at monthly clinic visits; patients were also encouraged to monitor blood pressure at home using an automated device. LVMI was determined by 2-dimensional echocardiography at baseline and after 1 and 2 years of treatment. QOL was assessed using the Medical Outcomes Study 36-Item Short-Form Health Survey. Electrocardiographic, laboratory, and QOL parameters were assessed at the beginning of treatment, and at 6 months, 1 year, and 2 years. RESULTS: One hundred seventy-four patients (87 men, 87 women) were enrolled in the study, and 168 completed it: 82 (42 men, 40 women; mean [SD] age, 52 [7] years) in the stevioside group and 86 (44 women, 42 men; mean age, 53 [7] years) in the placebo group. After 2 years, the stevioside group had significant decreases in mean (SD) SBP and DBP compared with baseline (SBP, from 150 [7.3] to 140 [6.8] mm Hg; DBP, from 95 [4.2] to 89 [3.2] mm Hg; P < 0.05) and compared with placebo (P < 0.05). Based on patients' records of self-monitored blood pressure, these effects were noted beginning approximately 1 week after the start of treatment and persisted throughout the study. There were no significant changes in body mass index or blood biochemistry, and the results of laboratory tests were similar in the 2 groups throughout the study. No significant difference in the incidence of adverse effects was noted between groups, and QOL scores were significantly improved overall with stevioside compared with placebo (P < 0.001). Neither group had a significant change in mean LVMI. However, after 2 years, 6 of 52 patients (11.5%) in the stevioside group had left ventricular hypertrophy (LVH), compared with 17 of 50 patients (34.0%) in the placebo group (P < 0.001). Of those who did not have LVH at baseline, 3 of 46 patients (6.5%) in the stevioside group had developed LVH after 2 years, compared with 9 of 37 patients (24.3%) in the placebo group (P < 0.001). CONCLUSIONS: In this 2-year study in Chinese patients with mild hypertension, oral stevioside significantly decreased SBP and DBP compared with placebo. QOL was improved, and no significant adverse effects were noted.
    Effects of stevioside on glucose transport activity in insulin-sensitive and insulin-resistant rat skeletal muscle.

    Lailerd N, Saengsirisuwan V, Sloniger JA, Toskulkao C, Henriksen EJ.

    Muscle Metabolism Laboratory, Department of Physiology, University of Arizona College of Medicine, Tuscon, USA.

    Stevioside (SVS), a natural sweetener extracted from Stevia rebaudiana, has been used as an antihyperglycemic agent. However, little is known regarding its potential action on skeletal muscle, the major site of glucose disposal. Therefore, the purpose of the present study was to determine the effect of SVS treatment on skeletal muscle glucose transport activity in both insulin-sensitive lean (Fa/-) and insulin-resistant obese (fa/fa) Zucker rats. SVS was administered (500 mg/kg body weight by gavage) 2 hours before an oral glucose tolerance test (OGTT). Whereas the glucose incremental area under the curve (IAUC(glucose)) was not affected by SVS in lean Zucker rats, the insulin incremental area under the curve (IAUC(insulin)) and the glucose-insulin index (product of glucose and insulin IAUCs and inversely related to whole-body insulin sensitivity) were decreased (P<.05) by 42% and 45%, respectively. Interestingly, in the obese Zucker rat, SVS also reduced the IAUC(insulin) by 44%, and significantly decreased the IAUC(glucose) (30%) and the glucose-insulin index (57%). Muscle glucose transport was assessed following in vitro SVS treatment. In lean Zucker rats, basal glucose transport in type I soleus and type IIb epitrochlearis muscles was not altered by 0.01 to 0.1 mmol/L SVS. In contrast, 0.1 mmol/L SVS enhanced insulin-stimulated (2 mU/mL) glucose transport in both epitrochlearis (15%) and soleus (48%). At 0.5 mmol/L or higher, the SVS effect was reversed. Similarly, basal glucose transport in soleus and epitrochlearis muscles in obese Zucker rats was not changed by lower doses of SVS (0.01 to 0.1 mmol/L). However, these lower doses of SVS significantly increased insulin-stimulated glucose transport in both obese epitrochlearis and soleus (15% to 20%). In conclusion, acute oral SVS increased whole-body insulin sensitivity, and low concentrations of SVS (0.01 to 0.1 mmol/L) modestly improved in vitro insulin action on skeletal muscle glucose transport in both lean and obese Zucker rats. These results indicate that one potential site of action of SVS is the skeletal muscle glucose transport system.
    Last edited by pogue; 11-11-2006 at 06:12 AM.
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    Post Stevia (Continued)

    Stevia (Continued)

    Stevioside.

    Geuns JM.

    Laboratory of Plant Physiology, Catholic University of Leuven, Kasteelpark Arenberg 31, B 3001 Leuven, Belgium. jan.geuns@bio.kuleuven.ac.be

    Stevioside is a natural sweetener extracted from leaves of Stevia rebaudiana (Bertoni) Bertoni. The literature about Stevia, the occurrence of its sweeteners, their biosynthetic pathway and toxicological aspects are discussed. Injection experiments or perfusion experiments of organs are considered as not relevant for the use of Stevia or stevioside as food, and therefore these studies are not included in this review. The metabolism of stevioside is discussed in relation with the possible formation of steviol. Different mutagenicity studies as well as studies on carcinogenicity are discussed. Acute and subacute toxicity studies revealed a very low toxicity of Stevia and stevioside. Fertility and teratogenicity studies are discussed as well as the effects on the bio-availability of other nutrients in the diet. The conclusion is that Stevia and stevioside are safe when used as a sweetener. It is suited for both diabetics, and PKU patients, as well as for obese persons intending to lose weight by avoiding sugar supplements in the diet. No allergic reactions to it seem to exist.
    Metabolism of stevioside and rebaudioside A from Stevia rebaudiana extracts by human microflora.

    Gardana C, Simonetti P, Canzi E, Zanchi R, Pietta P.

    Department of Food Science and Microbiology, Division of Human Nutrition, University of Milan, Via Celoria 2, 20133 Milan, Italy.

    Stevia rebaudiana standardized extracts (SSEs) are used as natural sweeteners or dietary supplements in different countries for their content of stevioside or rebaudioside A. These compounds possess up to 250 times the sweetness intensity of sucrose, and they are noncaloric and noncariogenic sweeteners. The aim of this study was to investigate the in vitro transformation of stevioside and rebaudioside A after incubation with human microflora, the influence of these sweeteners on human microbial fecal community and which specific groups metabolize preferentially stevioside and rebaudioside A. The experiments were carried out under strict anaerobic conditions in batch cultures inoculated with mixed fecal bacteria from volunteers. The hydrolysis was monitored by HPLC coupled to photodiode array and mass spectrometric detectors. Isolated bacterial strains from fecal materials incubated in selective broths were added to stevioside and rebaudioside A. These sweeteners were completely hydrolyzed to their aglycon steviol in 10 and 24 h, respectively. Interestingly, the human intestinal microflora was not able to degrade steviol. Furthermore, stevioside and rebaudioside A did not significantly influence the composition of fecal cultures; among the selected intestinal groups, bacteroides were the most efficient in hydrolyzing Stevia sweeteners to steviol.
    Absorption and metabolism of glycosidic sweeteners of stevia mixture and their aglycone, steviol, in rats and humans.

    Koyama E, Sakai N, Ohori Y, Kitazawa K, Izawa O, Kakegawa K, Fujino A, Ui M.

    Kashima Laboratory, Mitsubishi Chemical Safety Institute Ltd., 14 Sunayama, Hasaki-machi, Ibaraki, 314-0255, Kashima-gun, Japan. e-koyama@ankaken.co.jp

    Stevia mixture, sweeteners extracted from the leaves of Stevia rebaudiana Bertoni, consists mainly of the glycosides of the diterpene derivative steviol. The aims of this study were to investigate the absorption (in rats) and the hepatic metabolism (in rats and humans) of both stevia mixture and steviol. Absorption was investigated both in vivo and ex vivo. In ex vivo experiments using the rat everted sac method, no absorption of stevia mixture was observed, but significant absorption of steviol was noted (equivalent to approximately 70% of the absorption reference- salicylic acid- value). In the in vivo experiment, rats received a single oral administration of either steviol or stevia mixture; a peak steviol concentration in plasma was observed 15 min after its oral administration, demonstrating rapid absorption. However, after oral administration of stevia mixture, the steviol concentration in plasma increased steadily over 8 h, suggesting that stevia mixture components are first degraded and then absorbed as steviol in the rat intestine. Steviol metabolism in humans and rats was examined by incubating steviol with liver microsomes from the two species. Oxidative (monohydroxy and dihydroxy) metabolites of steviol were observed by LC-ESI/MS after incubation with both human and rat liver microsomes. The intrinsic clearance of steviol in human liver microsomes was 4-times lower than that found in rat liver microsomes. In conclusion, this study suggests that there are no major species differences in steviol hepatic metabolism between rats and humans. Absorption from the human intestine can be predicted to occur in an analogous manner to that from the rat intestine.
    Acute toxicity of stevioside, a natural sweetener, and its metabolite, steviol, in several animal species.

    Toskulkao C, Chaturat L, Temcharoen P, Glinsukon T.

    Department of Physiology, Faculty of Science, Mahidol University, Bangkok, Thailand.

    The acute toxicity of stevioside and steviol (a product of enzymatic hydrolysis of stevioside) was investigated in three animal species including rat, mouse and hamster. The susceptibility to stevioside and steviol acute toxicity in both sexes of these animal species was compared. The animals were treated intragastrically with stevioside or steviol and general signs and symptoms were observed. The numbers of dead animals were recorded within a period of 14 days after administration for estimation of LD50. Stevioside at a dose as high as 15 g/kg BW was not lethal to either mice, rats or hamsters. Hamsters were found to be more susceptible to steviol than rats or mice. LD50 values of steviol in hamsters were 5.20 and 6.10 g/kg BW for males and females, respectively. In rats and mice, LD50 values of steviol were higher than 15 g/kg BW in both sexes. Histopathological examination in the kidney of hamsters induced by steviol revealed severe degeneration of the proximal tubular cells. These structural alterations were correlated with the increases in serum blood urea nitrogen (BUN) and creatinine. Therefore, the possible cause of death induced by steviol might be due to acute renal failure.
    Effect of stevioside on growth and reproduction.

    Yodyingyuad V, Bunyawong S.

    Chulalongkorn University Primate Research Centre, Faculty of Science, Bangkok, Thailand.

    The effect on growth and reproduction in hamsters of stevioside, which is extracted from stevia leaves (Stevia rebaudiana Bertoni) and is currently used as a non-caloric sweetener, was investigated. Four groups of 20 one-month-old hamsters (10 males and 10 females) were daily force-fed with stevioside (0.0, 0.5, 1.0 and 2.5 g/kg body wt/day, respectively). No abnormalities were found in growth and fertility in both sexes. All males mated females efficiently and successfully. Females showed normal 4-day oestrus cycles and became pregnant after mating. Each female was mated and allowed to bear three litters during the period of experiment. The duration of pregnancy, number of fetuses, as well as number of young delivered each time from females in the experimental groups were not significantly different from those in the control group. The young F1 and F2 hamsters continuously receiving stevioside via drinking water until one month old and daily force-fed afterwards at the same doses as their parents showed normal growth and fertility. Histological examinations of reproductive tissues from all three generations revealed no evidence of abnormality which could be linked to the effects of consuming stevioside. We conclude that stevioside at a dose as high as 2.5 g/kg body wt/day affects neither growth nor reproduction in hamsters.
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    Post Acesulfame

    Acesulfame

    You would think they would name these sweeteners something less scary, or easy to pronounce. It might help with their public relations. Anyway...

    Acesulfame is a derivative of a potassium salt 6-methyl-1,2,3- oxathiazine-4(3H)-one-2,2-dioxide. Just don't try asking for that at Walmart. Acesulfame is a relatively new sweetener, and is 200 times sweeter than sugar. You will typically find acesulfame being mixed with aspartame to provide a cleaner taste, with less aftertaste. I also assume it is much cheaper. Like sucralose, acesulfame is not processed in the body, it is simply ingested and excreted.

    There has been some question about the safety of acesulfame because there hasn't been that many toxicity studies done on it. The ADI is 15mg/kg of bodyweight.

    Acesulfame from the Wikipedia
    Acesulfame from Calorie Control
    All you need to know on Acesulfame by AAFP
    Quotes from Doctors on Acesulfame concerns

    I had quite a bit of trouble finding any published studies on data in humans alone. In fact, I didn't find any, which concerns me a little. Although, the safety data seems to be available, I could not find it. I would have to say to avoid acesulfame as much as possible. I wouldn't be overly concerned about using it, but the lack of data on it worries me.
    In vivo cytogenetic studies on blends of aspartame and acesulfame-K.

    Mukhopadhyay M, Mukherjee A, Chakrabarti J.

    Centre for Advanced Studies on Cell and Chromosome Research, Department of Botany, University of Calcutta, 35 Ballygunge Circular Road, Calcutta 700 019, India.

    Aspartame and acesulfame-K, non-nutritive sweeteners, are permitted individually in diets and beverages. These sweeteners of different classes, used in combination, have been found to possess a synergistic sweetening effect. Whether they also have a synergistic genotoxic effect is unknown. Swiss Albino male mice were exposed to blends of aspartame (3.5, 35, 350mg/kg body weight) and acesulfame-K (1.5, 15 and 150mg/kg body weight) by gavage. Bone marrow cells isolated from femora were analysed for chromosome aberrations. Statistical analysis of the results show that aspartame in combination with acesulfame-K is not significantly genotoxic.
    Last edited by pogue; 11-11-2006 at 06:12 AM.
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    Post Saccharin (Sweet 'n Low)

    Saccharin

    Saccharin is the gold standard of artificial sweeteners, it's the original. Saccharin has been around since 1879, but you probably know it as the little pink packets on your table at ever restaurant. It is 300 times as sweet as sucrose.

    There has been some controversy in the past showing that saccharin gave rats urinary cancer. However, it was later shown that any type of cancer would only occur at high doses. This one of those cases where it depends on who you ask as to why there is a controversy, but in reality - saccharin is not found in very much anymore in any type of processed food or drink. Saccharin has fallen out of favor, since the newer artificial sweeteners have emerged. Saccharin is considered more of a first generation artificial sweetener, and doesn't have a taste similar to sugar. It is very sweet and can have a bitter taste if too much is used. You will find most people use saccharin today to flavor their coffee, and little else. The ADI on saccharin is 5mg/kg. Saccharin is not recommended for pregnant or breast feeding women.

    Saccharin from the Wikipedia
    Calorie Control info on Saccharin
    CSPI Reports on Saccharin

    A data-derived safety (uncertainty) factor for the intense sweetener, saccharin.

    Renwick AG.

    Clinical Pharmacology Group, University of Southampton, Bassett Crescent East, UK.

    An increased incidence of bladder cancer is found when male rats are fed high dietary concentrations of sodium saccharin (3% or more) from birth. This toxicity has been used as the basis for the development of a data-derived safety factor. Such an effect would attract an extra factor (10-fold) for nature of toxicity and in the absence of other data would result in a high overall safety factor. However the extensive mechanistic database on sodium saccharin allows an assessment of the potential relevance of the effect for humans. In addition the effect is only seen under specific conditions in rats, i.e. largely with the sodium salt and with a commercial rat diet. The effect is not related to the concentration of saccharin in the rat urine or bladder so that toxicokinetic considerations are simplified. The extensive animal database allows the determination of data-derived factors for inter-species differences in both toxicokinetics and toxicodynamics. Based on this analysis an overall safety factor of 50 (which includes the factor of 10 for severity of effect) would appear appropriate at the present time. This factor, and the ADI which would result from its application, are consistent with the absence of an association between the consumption of artificial sweeteners and bladder cancer in humans.
    Update on artificial sweeteners and bladder cancer.

    Elcock M, Morgan RW.

    Environmental Health Strategies, Inc., Redwood City, California 94065.

    Review of the most recent epidemiologic studies indicates there is no detectable association between artificial sweetener consumption and bladder cancer. The summary relative risk from a meta-analysis of all case-control studies approaches unity (RR .97). This analysis, in combination with new evidence for a unique mechanism of saccharin carcinogenicity in the male rat, leads to the conclusion that saccharin is not related to bladder cancer in humans.
    The health risks of saccharin revisited.

    Ellwein LB, Cohen SM.

    South Dakota State University, Brookings.

    Almost from its discovery in 1879, the use of saccharin as an artificial, non-nutritive sweetener has been the center of several controversies regarding potential toxic effects, most recently focusing on the urinary bladder carcinogenicity of sodium saccharin in rats when fed at high doses in two-generation studies. No carcinogenic effect has been observed in mice, hamsters, or monkeys, and numerous epidemiological studies provide no clear or consistent evidence to support the assertion that sodium saccharin increases the risk of bladder cancer in the human population. Mechanism of action studies in the one susceptible species, the rat, continue to provide information useful in assessing potential risk to the human from saccharin consumption. Unlike typical carcinogens which interact with DNA, sodium saccharin is not genotoxic, but leads to an increase in cell proliferation of the urothelium, the only target tissue. It also appears that the effect of saccharin is modified by the salt form in which it is administered, despite equivalent concentrations of saccharin in the urine. The chemical form of saccharin in the urine is unaffected, and there is no evidence for a specific cell receptor for the saccharin molecule. Changes in several urinary parameters, such as pH, sodium, protein, silicates, volume, and others, appear to influence the reaction of the urothelium to sodium saccharin administration. Silicon-containing precipitate and/or crystals appear to be generated in the urine under specific circumstances, acting as microabrasive, cytotoxic material. Using a mathematical model of carcinogenesis, which encompasses the temporal dynamics and complexity of the process at a cellular level, including spontaneous genetic transitions, it has been shown that the effects of sodium saccharin can be explained entirely in terms of its non-genotoxic influence on cell proliferation. In interpreting these analytical studies in the human context, particularly as they pertain to the urinary milieu which appears to be pivotal in the effect of sodium saccharin, we are led to the conclusion that there is a threshold effect in male rats and that an effect on the human urothelium is unlikely at even the highest levels of human consumption.
    Last edited by pogue; 11-11-2006 at 06:14 AM.
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    Post Sugar Alcohols

    Sugar Alcohols

    Contary to the name, sugar alcohols don't get you drunk. Sugar alcohols are essentially just sugar where the chemical composition has been changed, so it still tastes sweet, but it won't influence blood sugar levels. Some common sugar alcohols are mannitol, sorbitol, xylitol, maltitol and lactitol. They are finding there way into everything from cookies and ice cream to tooth paste. Sugar alcohols tend to be more expensive than the other artifical sweetners on the market, but they can be easy to bake with.

    The main complaint about sugar alcohols is that they can cause a laxative effect in users who eat too much of them.

    Sugar Alcohols from Wikipedia

    These are the values I have seen reported by FDA from caloricontrolcounsel for various polyols

    3.0 calories per gram hydrogenated starch hydrolysates
    2.6 calories per gram sorbitol
    2.4 calories per gram xylitol
    2.1 calories per gram maltitol
    2.0 calories per gram isomalt
    2.0 calories per gram lactitol
    1.6 calories per gram mannitol
    0.2 calories per gram erythritol

    This article is incomplete - it will be finished in the near future. If anyone has any good information on sugar alcohols, please PM it to me, thanks.
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  15. #15
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    Cool

    Comments & Questions welcome.
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  16. #16
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    thanks for this great info, pogue.

    i've read a somewhat informal analysis of the correlation between reporting of aspartame's adverse effects and the funding source of the studies. veerrry interesting bias.. it's not an issue with me anyway, because i just use real friggin sugar, honey, & syrups.

    keep up the good work.

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    Originally posted by alan aragon
    thanks for this great info, pogue.

    i've read a somewhat informal analysis of the correlation between reporting of aspartame's adverse effects and the funding source of the studies. veerrry interesting bias.. it's not an issue with me anyway, because i just use real friggin sugar, honey, & syrups.

    keep up the good work.
    I couldn't find any studies within the last decade involving any dangers with aspartame. There were a few in the early 80s when it first came out with some questions about animal data and so forth, but I really didn't find them all that relevant.
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  18. #18
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    Alan what is your take on Stevia compared to Splenda?
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    Originally posted by pogue
    I couldn't find any studies within the last decade involving any dangers with aspartame. There were a few in the early 80s when it first came out with some questions about animal data and so forth, but I really didn't find them all that relevant.
    you better look closer at the research pertaining specifically to aspartame intake and individuals susceptible to headaches. sure, you might not find accross-the-board culpability, but enough to warrant concern. i'll post in a sec.

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    Originally posted by Sixpack
    Alan what is your take on Stevia compared to Splenda?
    Sixpack
    both relatively harmless, especially in the amounts typically ingested.. i've never tried stevia personally, but i've heard certain amounts of it can have a slightly bitter edge. i personally avoid artificial sweeteners despite their safety profiles, but that's just me.

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    aspartame & headache:
    _______________

    EFFECT IN HEADACHE-PRONE SUBSET:

    Neurology. 1994 Oct;44(10):1787-93. Aspartame ingestion and headaches: a randomized crossover trial. Van den Eeden SK, Koepsell TD, Longstreth WT Jr, van Belle G, Daling JR, McKnight B.

    Department of Epidemiology, School of Public Health and Community Medicine, University of Washington, Seattle 98195.

    To examine whether ingestion of aspartame is associated with headaches, we conducted a double-blind crossover study using volunteers with self-identified headaches after using aspartame. Of the 32 subjects randomized to receive aspartame (approximately 30 mg/kg/d) and placebo in a two-treatment, four-period crossover design, 18 completed the full protocol, seven completed part of the protocol before withdrawing due to adverse effects, three withdrew for other reasons, two were lost to follow-up, one was withdrawn due to noncompliance, and one withdrew and gave no reason. Each experimental period was 7 days long. Subjects reported headaches on 33% of the days during aspartame treatment, compared with 24% on placebo treatment (p = 0.04). Subjects who were "very sure" prior to the study that aspartame triggered some of their headaches reported larger treatment differences (aspartame = 0.37 headache-days, placebo = 0.18 headache-days; p < 0.001) than subjects who were "somewhat sure" (aspartame = 0.29 headache-days, placebo = 0.22 headache-days; p = 0.51) or "not sure" (aspartame = 0.33 headache-days, placebo = 0.39 headache-days; p = 0.51). There was no significant treatment difference in the length or intensity of headaches or in the occurrence of side effects associated with the headaches. This experiment provides evidence that, among individuals with self-reported headaches after ingestion of aspartame, a subset of this group report more headaches when tested under controlled conditions. It appears that some people are particularly susceptible to headaches caused by aspartame and may want to limit their consumption.


    NO EFFECT:

    N Engl J Med. 1987 Nov 5;317(19):1181-5. Aspartame and susceptibility to headache.

    Schiffman SS, Buckley CE 3rd, Sampson HA, Massey EW, Baraniuk JN, Follett JV, Warwick ZS.

    Department of Psychiatry, Duke University, Durham, N.C. 27710.

    We performed a double-blind crossover trial of challenges with 30 mg of aspartame per kilogram of body weight or placebo in 40 subjects who reported having headaches repeatedly after consuming products containing aspartame. The incidence rate of headache after aspartame (35 percent) was not significantly different from that after placebo (45 percent) (P less than 0.50). No serious reactions were observed, and the incidence of symptoms other than headache following aspartame was also equivalent to that after placebo. No treatment-related effects were detected in vital signs, blood pressure, or plasma concentrations of cortisol, insulin, glucagon, histamine, epinephrine, or norepinephrine. Most of the subjects were well educated and overweight and had a family or personal history of allergic reactions. The subjects who had headaches had lower plasma concentrations of norepinephrine (P less than 0.0002) and epinephrine (P less than 0.02) just before the development of headache. We conclude that in this population, aspartame is no more likely to produce headache than placebo.

    EFFECT:

    Headache. 1989 Feb;29(2):90-2. Related Articles, Links


    Aspartame as a dietary trigger of headache.

    Lipton RB, Newman LC, Cohen JS, Solomon S.

    Many dietary factors have been implicated as possible precipitants of headache. There have been recent differences of opinion with regard to the effect of the artificial sweetener aspartame as a precipitant of headache. To assess the importance of aspartame as a dietary factor in headache, 190 consecutive patients of the Montefiore Medical Center Headache Unit were questioned about the effect of alcohol, carbohydrates and aspartame in triggering their headaches. Of the 171 patients who fully completed the survey, 49.7 percent reported alcohol as a precipitating factor, compared to 8.2 percent reporting aspartame and 2.3 percent reporting carbohydrates. Patients with migraine were significantly more likely to report alcohol as a triggering factor and also reported aspartame as a precipitant three times more often than those having other types of headache. The conflicting results of two recent placebo-control studies of aspartame and headache are discussed. We conclude that aspartame may be an important dietary trigger of headache in some people.

    _______________

    as expected, the headache-aspartame connection is not an accoss-the-board phenomenon, but i would personally advise against headache or migraine-prone individuals using aspartame containing products, especially since there are other alternatives that have ZERO implications in headache etiology.
    Last edited by alan aragon; 06-22-2004 at 04:49 PM.

  22. #22
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    Originally posted by alan aragon
    as expected, the headache-aspartame connection is not an accoss-the-board phenomenon, but i would personally advise against headache or migraine-prone individuals using aspartame containing products, especially since there are other alternatives that have ZERO implications in headache etiology.
    Anything is possible, but there can be a lot of things that cause headaches.

    Clin Exp Allergy. 2000 May;30(5):739-43.
    Why do some dietary migraine patients claim they get headaches from placebos?

    Strong FC 3rd.

    Departamento de Ciencia de Alimentos, Faculdade de Engenharia de Alimentos, Universidade Estadual de Campinas, SP, Brasil.

    Aspartame is not neurotoxic, so if people are experiencing headaches, then they would obviously want to stop using it. But it is not physically harmful.

    Related studies on Aspartame & Headaches: http://www.ncbi.nlm.nih.gov/entrez/q...om_uid=7936222
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    Aspartame

    I have been anti artificial sweetners for some time now.

    I am at work and dont have my studies in front of me so I will wing it with Aspartame here:

    Aspartate and Glutamate act as neurotransmitters in the brain by allowing the transmission of information from neuron to neuron. Too much Aspartate or Glutamate in the brain kills certain neurons by allowing the influx of too much calcium into the cells. The influx triggers excessive amounts of free radicals which kill cells. The neural cell damage that can be caused by excessive aspartate and glutamate is why they are referred to as excitotoxins. They excite or stimulate the neural cells to death.

    There is link there with the blood brain barrier, which is above my head.

    Memory issues as well. Searle The maker of Aspartame (Was Monsanto until Searle and Monsanto merged) in 1987 did and exstensive search for a drug to combact excitatory amino acid damage. Professer Olney (University Of Washinton) has been trying to get Searle to understand the dangers since 1971 (Also MSG).

    My opinion on Splenda is not very high either.

    I have tons of info on fake sweetners. Bottom line: They are chemicals. I see no need to put these things in my body.

    The tablesppon of syrup (pure) in my oats I KNOW will do know harm. I in good faith cannot tell anyone that artificial sweetners are safe.

    I wish I had more time for these debates
    Last edited by fitnessman; 06-22-2004 at 05:42 PM.
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    Also

    I know Alan will agree with this. Follow the money trail when it comes to any study. I have been removed from two this year at the University. Sometimes when you dont go along with the party line, they will just find someone who will.

    I just hope to GOD I get accepted for the beer lable testing research
    Psalm 121

  25. #25
    The Merciful alan aragon's Avatar
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    even though this quote is from a rather alarmist anti-aspartame site (dorway.com), it's unsettling nevertheless. there's many examples of this sort of struggle between science and the politics of industry:
    The FDA Commissioner made that decision even though FDA Investigators and Toxicologists were warning him about the dangers of aspartame. The Public Board of Inquiry made up of scientists, including the President of the American Association of Neuropathologists, voted unanimously against approval of aspartame. The FDA Commissioner's original team of scientific experts was against approval of aspartame because the brain tumor data was so "worrisome."

    Of course, soon after the FDA Commissioner approved aspartame for carbonated beverages, he took a consulting position with the PR firm for G.D. Searle (maker of aspartame at the time) at $1,000/day.

  26. #26
    The Merciful alan aragon's Avatar
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    Re: Also

    Originally posted by fitnessman
    I know Alan will agree with this. Follow the money trail when it comes to any study. I have been removed from two this year at the University. Sometimes when you dont go along with the party line, they will just find someone who will.

    I just hope to GOD I get accepted for the beer lable testing research
    W00F

    let me know whether that beer study confirms what i already know: newcastle rules!


  27. #27
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    first off, great post!! we'll have to keep it bumped like alan's posts! (you can never have too many GOOD QUALITY stickies)

    i dont know about you guys with your fancy-dancy studies, but cavemen didnt have artificial sweetners and they were totally ripped

    i try to avoid anything "artificial" and overly processed(except cheese, milk, oats and whey) regardless of how safe studies prove it to be

    i usually treat myself to some sugar free jelly (Saccharin+weird colours and flavors that cause cancer ) and maybe some splenda

    i reckon the colours and flavors in products are probly worse than the sweetners! maybe everyone should argue about that

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    Re: Aspartame

    Originally posted by fitnessman
    I have been anti artificial sweetners for some time now.

    I am at work and dont have my studies in front of me so I will wing it with Aspartame here:

    Aspartate and Glutamate act as neurotransmitters in the brain by allowing the transmission of information from neuron to neuron. Too much Aspartate or Glutamate in the brain kills certain neurons by allowing the influx of too much calcium into the cells. The influx triggers excessive amounts of free radicals which kill cells. The neural cell damage that can be caused by excessive aspartate and glutamate is why they are referred to as excitotoxins. They excite or stimulate the neural cells to death.
    Effect of aspartame and sucrose loading in glutamate-susceptible subjects.

    Stegink LD, Filer LJ Jr, Baker GL.

    It has been postulated that individuals reporting an idiosyncratic symptom response after glutamate ingestion might also experience such symptoms after aspartame ingestion. Such sensitive subjects might have been missed in earlier studies of aspartame. In the present study, six subjects reporting various symptoms after glutamate ingestion, but not after placebo, were administered aspartame (34 mg/kg body weight) or sucrose (1 g/kg body weight) dissolved in orange juice in a randomized, cross-over, double-blind study. No subject reported symptoms typical of a glutamate response after either sucrose or aspartame loading. One subject reported slight nausea approximately 1.5 h after aspartame ingestion, but indicated that the symptoms were not those of a glutamate response. Plasma phenylalanine and aspartate levels were similar to those noted in normal subjects administered identical doses of aspartame. The data indicate no effect of aspartame loading in glutamate-susceptible subjects.
    Also, if you will note in my first post there is a study showing aspartame to not be neurotoxic. I have not investigated this area of it, but I am familar with glutamate toxicity, which can be caused by several factors including ammonia, MSG, and arginine and glutamine overload.

    Originally posted by fitnessman
    Memory issues as well. Searle The maker of Aspartame (Was Monsanto until Searle and Monsanto merged) in 1987 did and exstensive search for a drug to combact excitatory amino acid damage. Professer Olney (University Of Washinton) has been trying to get Searle to understand the dangers since 1971 (Also MSG).
    I couldn't find much on this, except all "Abstract not available"

    High doses of aspartame have no effects on sensorimotor function or learning and memory in rats.

    Tilson HA, Hong JS, Sobotka TJ.

    Division of Neurotoxicology, Environmental Protection Agency, Research Triangle Park, NC 27711.

    L-Phenylalanine is actually a very cognative enhancing amino acid. It is often given to Parkisons patients to increase memory function, alleive depression, etc. Drugs such as l-deprenyl work through this same mechanism.

    Originally posted by fitnessman
    I have tons of info on fake sweetners. Bottom line: They are chemicals. I see no need to put these things in my body.
    If you would realize how much processing goes into turning sugar cane into sucrose, it's really nothing "natural" left about it, other than it's origin. The same goes for high fructose corn syrup, which causes significantly allergic reactions in people and an even higher insulin spike that regular sucrose.

    Originally posted by fitnessman
    The tablesppon of syrup (pure) in my oats I KNOW will do know harm. I in good faith cannot tell anyone that artificial sweetners are safe.
    High GI carbs definintely have their place, no one can argue that. It's when we use them all the time thats the problem.
    I don't neg/infract/ban if you disagree with me in a civil discussion on any topic. I don't claim to be an expert on any subject and can always be proven wrong. But good luck trying ;)

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  29. #29
    ALLMAX NUTRITION Sixpack's Avatar
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    Well if Die from having splenda and Divinci suger free (splenda brand)syrups then do a study on me lol ,
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  30. #30
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    Originally posted by taffer
    i reckon the colours and flavors in products are probly worse than the sweetners! maybe everyone should argue about that
    Those colors are very frightening. Some of them are actually made from crushed insect shells, and a lot have been recalled for adverse effects.
    I don't neg/infract/ban if you disagree with me in a civil discussion on any topic. I don't claim to be an expert on any subject and can always be proven wrong. But good luck trying ;)

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