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Diet Soda

Carbonated sweet water with minimal calories. Diet sodas may be beneficial to a diet due to satiety effects and displacing sugared sodas, and their health effects should be seen as a sum of the parts like Energy Drinks. Not inherently healthy or unhealthy.

Our evidence-based analysis on diet soda features 53 unique references to scientific papers.

Research analysis led by and reviewed by the Examine team.
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Research Breakdown on Diet Soda

1Components of Diet Soda

Common ingredients or characteristics of Diet Soda that may influence health include:

  • Artificial sweeteners such as Aspartame

  • Sweetening enhancers like Acesulfame-Potassium

  • Coloring (of which caramel coloring is of interest for colas)

  • Caffeine content

  • Carbonation and General pH (acidity)

Other ingredients may exist in certain diet sodas, and the label should be looked at to see what may be of concern to you. This page will cover general topics, and link to relevant and sourced FAQ pages.


Aspartame is the most widely used and controversial artifical sweetener currently on the market, and is implicated in a wide-variety of concerns.

Concern of aspartame appears to be overblown for the most part. Its ability to 'cause headaches' is not well known and highly confounded with placebo/hypochondriacs, as well as being an underresearched topic. FAQ

Despite being sweet, aspartame does not appear to increase appetite. In actuality, it may actually suppress appetite due to the amino acids that make up the structure of aspartame. FAQ

Aspartame also does not seem to be a large concern when it comes to spiking insulin in the dosages commonly consumed through diet soda. FAQ Subsequently, fat loss is not impaired with diet soda use and it can be a safe addition to a lifestyle designed to lose body fat. FAQ

3Acidity and Carbonation

The acidity of diet sodas are one of the legitimate concerns, as diet soda (and to a greater degree, regular soda) are risk factors for dental caries in children. Mentioned in this FAQ

4Caramel Coloring

Caramel coloring in some cola products (Coke, Pepsi) is due to a molecule called 4-methylimidazole (henceforth 4-MEI), which is produced during browning reactions[1] (not limited to cola). It has also been noted in Soy and Worcestershire sauce[2] as well as coffee[3] and dark beers,[4] although it is most well known for being in caramel soda.[5]

4-MEI appears to be involved in carcinogenesis, although its role is not clear. Toxicology studies in rats fed high doses of 4-MEI appear to indicate that it has carcinogenic (cancer-promoting) activities,[6] however some argue that it may be anti-carcinogenic when looking at other tumor colonies.[7] It should be noted that this review received funding from the 'American Beverage Association'.

When looking at the severity of 4-MEI exposure, an oral dosage of greater than 115-120mg/kg bodyweight daily over 106 weeks is associated with metabolic aberrations. Dosages below this do not appear to be much of a concern within this time frame.

The incidence of mononuclear cell leukemia at an oral dose of 250mg/kg bodyweight was significantly greater than control in females (dose not tested in males) and dosages above 115-120mg/kg bodyweight were associated with increased hepatocellular foci.[6] This high dose was also associated with a 25-fold decrease in mammary tumors as noted by Murray, FJ in a review on the topic.[7] Overall, there were no differences in mortality at any dosage, and body weight was decreased in the highest dosages.[6]

The mechanism of action may be acting as a co-carcinogen, by inhibiting an enzyme (in P450, CYP2E1) that metabolizes carcinogens.[8]

The dosage commonly found in soda is 250ppm max in the European Union[9] and is unregulated in the US; common levels found in soft drinks in the US range from 0.3-0.36mcg/mL of beverage,[1][4] which gives a range of 108-130mcg per 12 ounce beverage (375mL). One study estimated an intake of "2.3 and 5.7 mcg/kg body weight/day, in Europe and the United States, respectively"[4] Relatively small dosages when considering the level of 4-MEI that was significant in the rat toxicology study, measured in mg/kg bodyweight.

Assuming the highest human estimate (5.7mcg/kg daily) and the lowest animal estimate that resulted in difference than control (30mg/kg bodyweight in female rats for alveolar hyperplasia), there is a greater than 5,000-fold difference.

The most concern you should have from 4-methylimidazole, or 4-MEI, is how it can make your teeth look brown if you don't rinse your mouth.


  1. ^ a b Moon JK, Shibamoto T. Formation of carcinogenic 4(5)-methylimidazole in Maillard reaction systems. J Agric Food Chem. (2011)
  2. ^ Yamaguchi H, Masuda T. Determination of 4(5)-methylimidazole in soy sauce and other foods by LC-MS/MS after solid-phase extraction. J Agric Food Chem. (2011)
  3. ^ Lojková L, et al. Supercritical fluid extraction (SFE) of 4(5)-methylimidazole (4-MeI) and 2-acetyl-4(5)-(1,2,3,4)-tetrahydroxybutyl-imidazole (THI) from ground-coffee with high-performance liquid chromatographic-electrospray mass spectrometric quantification (HPLC/ESI-MS). Food Addit Contam. (2006)
  4. ^ a b c Assessment of 4-(5-)methylimidazole in soft drinks and dark beer.
  5. ^ Klejdus B, et al. Solid-phase extraction of 4(5)-methylimidazole (4MeI) and 2-acetyl-4(5)-(1,2,3,4-tetrahydroxybutyl)-imidazole (THI) from foods and beverages with subsequent liquid chromatographic-electrospray mass spectrometric quantification. J Sep Sci. (2006)
  6. ^ a b c Chan PC, et al. Toxicity and carcinogenicity studies of 4-methylimidazole in F344/N rats and B6C3F1 mice. Arch Toxicol. (2008)
  7. ^ a b Murray FJ. Does 4-methylimidazole have tumor preventive activity in the rat. Food Chem Toxicol. (2011)
  8. ^ Hargreaves MB, et al. Inhibition of p-nitrophenol hydroxylase in rat liver microsomes by small aromatic and heterocyclic molecules. Drug Metab Dispos. (1994)
  9. ^ Moretton C, et al. Quantification of 4-methylimidazole in class III and IV caramel colors: validation of a new method based on heart-cutting two-dimensional liquid chromatography (LC-LC). J Agric Food Chem. (2011)
  10. Spiers PA, et al. Aspartame: neuropsychologic and neurophysiologic evaluation of acute and chronic effects. Am J Clin Nutr. (1998)
  11. Ford HE, et al. Effects of oral ingestion of sucralose on gut hormone response and appetite in healthy normal-weight subjects. Eur J Clin Nutr. (2011)
  12. Ma J, et al. Effect of the artificial sweetener, sucralose, on gastric emptying and incretin hormone release in healthy subjects. Am J Physiol Gastrointest Liver Physiol. (2009)
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  14. Steinert RE, et al. Effects of carbohydrate sugars and artificial sweeteners on appetite and the secretion of gastrointestinal satiety peptides. Br J Nutr. (2011)
  15. Møller SE. Effect of aspartame and protein, administered in phenylalanine-equivalent doses, on plasma neutral amino acids, aspartate, insulin and glucose in man. Pharmacol Toxicol. (1991)
  16. Wolf-Novak LC, et al. Aspartame ingestion with and without carbohydrate in phenylketonuric and normal subjects: effect on plasma concentrations of amino acids, glucose, and insulin. Metabolism. (1990)
  17. Horwitz DL, McLane M, Kobe P. Response to single dose of aspartame or saccharin by NIDDM patients. Diabetes Care. (1988)
  18. Teff KL, Devine J, Engelman K. Sweet taste: effect on cephalic phase insulin release in men. Physiol Behav. (1995)
  19. Malaisse WJ, et al. Effects of artificial sweeteners on insulin release and cationic fluxes in rat pancreatic islets. Cell Signal. (1998)
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  21. Storey ML, Forshee RA, Anderson PA. Beverage consumption in the US population. J Am Diet Assoc. (2006)
  22. Stellman SD, Garfinkel L. Artificial sweetener use and one-year weight change among women. Prev Med. (1986)
  23. Fowler SP, et al. Fueling the obesity epidemic? Artificially sweetened beverage use and long-term weight gain. Obesity (Silver Spring). (2008)
  24. Mattes RD, Popkin BM. Nonnutritive sweetener consumption in humans: effects on appetite and food intake and their putative mechanisms. Am J Clin Nutr. (2009)
  25. Prevalence of overweight, obesity and extreme obesity among adults: United States, trends 1960-62 through 2005-2006.
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  31. Okuno G, et al. Glucose tolerance, blood lipid, insulin and glucagon concentration after single or continuous administration of aspartame in diabetics. Diabetes Res Clin Pract. (1986)
  32. Just T, et al. Cephalic phase insulin release in healthy humans after taste stimulation. Appetite. (2008)
  33. Oyama Y, et al. Carrier-mediated transport systems for glucose in mucosal cells of the human oral cavity. J Pharm Sci. (1999)
  34. Carlson HE, Shah JH. Aspartame and its constituent amino acids: effects on prolactin, cortisol, growth hormone, insulin, and glucose in normal humans. Am J Clin Nutr. (1989)
  35. Rogers PJ, Blundell JE. Reanalysis of the effects of phenylalanine, alanine, and aspartame on food intake in human subjects. Physiol Behav. (1994)
  36. Porikos KP, Booth G, Van Itallie TB. Effect of covert nutritive dilution on the spontaneous food intake of obese individuals: a pilot study. Am J Clin Nutr. (1977)
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