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Artificial Sweetners

Saccharin

"Saccharin is the gold standard of artifical sweetners, 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 artifical sweetners have emerged. Saccharin is considered more of a first generation artifical sweetner, 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."
 
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.
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and

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.
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Having said that, I am not sucking down buckets of saccharin.
 
I agree with you that it's not conclusive and that there is plenty of evidence suggesting saccharin may be perfectly safe -- but it's not unanimous and the potential risks scare the shit out of me.

Mutat Res. 2002 Aug 26;519(1-2):103-19.

The comet assay with 8 mouse organs: results with 39 currently used food additives.

Sasaki YF, Kawaguchi S, Kamaya A, Ohshita M, Kabasawa K, Iwama K, Taniguchi K, Tsuda S.

Laboratory of Genotoxicity, Faculty of Chemical and Biological Engineering, Hachinohe National College of Technology, Tamonoki Uwanotai 16-1, Aomori 039-1192, Japan. [email protected]

We determined the genotoxicity of 39 chemicals currently in use as food additives. They fell into six categories-dyes, color fixatives and preservatives, preservatives, antioxidants, fungicides, and sweeteners. We tested groups of four male ddY mice once orally with each additive at up to 0.5xLD(50) or the limit dose (2000mg/kg) and performed the comet assay on the glandular stomach, colon, liver, kidney, urinary bladder, lung, brain, and bone marrow 3 and 24h after treatment. Of all the additives, dyes were the most genotoxic. Amaranth, Allura Red, New Coccine, Tartrazine, Erythrosine, Phloxine, and Rose Bengal induced dose-related DNA damage in the glandular stomach, colon, and/or urinary bladder. All seven dyes induced DNA damage in the gastrointestinal organs at a low dose (10 or 100mg/kg). Among them, Amaranth, Allura Red, New Coccine, and Tartrazine induced DNA damage in the colon at close to the acceptable daily intakes (ADIs). Two antioxidants (butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT)), three fungicides (biphenyl, sodium o-phenylphenol, and thiabendazole), and four sweeteners (sodium cyclamate, saccharin, sodium saccharin, and sucralose) also induced DNA damage in gastrointestinal organs. Based on these results, we believe that more extensive assessment of food additives in current use is warranted.
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Increasing brain tumor rates: is there a link to aspartame?

Olney JW, Farber NB, Spitznagel E, Robins LN.

Department of Psychiatry, Washington University Medical School, St. Louis, MO 63110, USA.

In the past two decades brain tumor rates have risen in several industrialized countries, including the United States. During this time, brain tumor data have been gathered by the National Cancer Institute from catchment areas representing 10% of the United States population. In the present study, we analyzed these data from 1975 to 1992 and found that the brain tumor increases in the United States occurred in two distinct phases, an early modest increase that may primarily reflect improved diagnostic technology, and a more recent sustained increase in the incidence and shift toward greater malignancy that must be explained by some other factor(s). Compared to other environmental factors putatively linked to brain tumors, the artificial sweetener aspartame is a promising candidate to explain the recent increase in incidence and degree of malignancy of brain tumors. Evidence potentially implicating aspartame includes an early animal study revealing an exceedingly high incidence of brain tumors in aspartame-fed rats compared to no brain tumors in concurrent controls, the recent finding that the aspartame molecule has mutagenic potential, and the close temporal association (aspartame was introduced into US food and beverage markets several years prior to the sharp increase in brain tumor incidence and malignancy). We conclude that there is need for reassessing the carcinogenic potential of aspartame.


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8939194&dopt=Abstract
 
Adverse reactions to aspartame: double-blind challenge in patients from a vulnerable population.

Walton RG, Hudak R, Green-Waite RJ.

Department of Psychiatry, Northeastern Ohio Universities College of Medicine, Youngstown.

This study was designed to ascertain whether individuals with mood disorders are particularly vulnerable to adverse effects of aspartame. Although the protocol required the recruitment of 40 patients with unipolar depression and a similar number of individuals without a psychiatric history, the project was halted by the Institutional Review Board after a total of 13 individuals had completed the study because of the severity of reactions within the group of patients with a history of depression. In a crossover design, subjects received aspartame 30 mg/kg/day or placebo for 7 days. Despite the small n, there was a significant difference between aspartame and placebo in number and severity of symptoms for patients with a history of depression, whereas for individuals without such a history there was not. We conclude that individuals with mood disorders are particularly sensitive to this artificial sweetener and its use in this population should be discouraged.


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Retrieve&list_uids=8373935&dopt=Abstract
 
Possible neurologic effects of aspartame, a widely used food additive.

Maher TJ, Wurtman RJ.

Department of Pharmacology, Massachusetts College of Pharmacy, Boston 02115.

The artificial sweetener aspartame (L-aspartyl-L-phenylalanyl-methyl ester), is consumed, primarily in beverages, by a very large number of Americans, causing significant elevations in plasma and, probably, brain phenylalanine levels. Anecdotal reports suggest that some people suffer neurologic or behavioral reactions in association with aspartame consumption. Since phenylalanine can be neurotoxic and can affect the synthesis of inhibitory monoamine neurotransmitters, the phenylalanine in aspartame could conceiveably mediate neurologic effects. If mice are given aspartame in doses that elevate plasma phenylalanine levels more than those of tyrosine (which probably occurs after any aspartame dose in humans), the frequency of seizures following the administration of an epileptogenic drug, pentylenetetrazole, is enhanced. This effect is simulated by equimolar phenylalanine and blocked by concurrent administration of valine, which blocks phenylalanine's entry into the brain. Aspartame also potentiates the induction of seizures by inhaled fluorothyl or by electroconvulsive shock. Perhaps regulations concerning the sale of food additives should be modified to require the reporting of adverse reactions and the continuing conduct of mandated safety research.


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Retrieve&list_uids=3319565&dopt=Abstract
 
Stevia and xylitol have both been shown to be great for dental hygiene. Stevia probably helps reduce plaque buildup, and xylitol probably helps prevent and even reverse tooth decay.

P.S. the whole aspartame as an excitotoxin thing is bull.
 
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