Guide to Sucralose

Sucralose is a commonly used artificial food sweetener that provides no nutrition. It’s about 600 times as sweet as table sugar and the majority of it is not absorbed by the body. It has been licensed for use as a sweetener in Japan since 1999.

Sucralose is a trichlorinated sucrose molecule; i.e. it’s a form of sucrose (table sugar) that’s been altered chemically. Sucralose is very stable: it’s not affected by heat or light and is unaffected by a broad range of pH conditions. As well as its reliable stability, sucralose is also favoured in respect of taste and texture and it has no negative after-taste; therefore, sucralose is a great choice both for baking and for commercial products that require a longer shelf life.

As well as Japan, sucralose is licensed for use in the USA, Australia and EU; in fact over 80 countries in total. Indeed, it is experiencing increasing popularity as a sweetener when compared to other commonly used artificial sweeteners like aspartame, acesulfame K and saccharin.

What happens to Sucralose after consumption?

After consuming sucralose, the majority of it is not absorbed into the body and passes through the digestive system to be excreted in faeces. As sucralose is poorly absorbed by the digestive tract, only 5 to 20% of it actually enters the blood. The remainder is removed through urine, essentially unchanged and none is stored in tissues[1]. Therefore, sucralose is actually only present in the body for a short time after consumption.

The Evidence

Although sucralose has no actual direct health benefits, as it’s a nonnutritive alternative to sugar, it has a number of indirect benefits associated with this use. The consumption of sugar is well known to be associated with dental caries (tooth decay) and periodontal (gum) disease. Using sucralose reduces sugar intake with the consequential benefits to dental health and it has thus been shown to be non-cariogenic[2].

Sucralose, being a nonnutritive sweetener, is used in many low calorie products. It’s been shown to have no effect on hunger signalling and does not initiate an insulin response[4].

Some people claim that sucralose alters the amount and quality of the good bacteria that reside symbiotically in our gut. This claim is mostly based around a 2008 study by Abou-Donia et al[5]. It’s also been claimed that sucralose limits the absorption of some therapeutic drugs rendering them less effective[5, 6]. There are further suggestions that sucralose decomposes during baking and releases potentially toxic compounds called chloropropanols[6].

However, the Abou-Donia et al 2008 paper has been debunked by many including an Expert Panel who found that the study was deficient in several critical areas and stated that its results could be interpreted as implicative that there are any problems with sucralose ingestion[7]. The Abou-Donia et al study and the Schiffman & Rother (2013) review - and it should be noted that both these papers were published in the same journal - based their findings on rats, not humans, and these rats were fed large amounts based on their body weight[5, 6]. Indeed, they were actually fed the brand of sucralose Splenda which contains maltodextrin and dextrose as fillers alongside sucralose, so any ill effect could have be due to these high glycaemic index carbohydrates and not the sucralose. Other studies have indicated that there is no change in gut function including to gut microflora following sucralose consumption[1, 7, 8].

One other claim - a claim that is also made about some other non-caloric sweeteners - is that there is an altered insulin response, blood sugar level and, in turn, appetite following consumption of sucralose. There are claims that this is a learned sensory response from associating the sweet taste of sucralose with sugar which leads to the insulin response[6]. It’s well known that high sugar intakes only lead to short term satiety and this is followed by a subsequent increase in appetite and it has been claimed that the same happens following sucralose ingestion. However, this is not the case and the sensation of appetite is very complex involving a number of hormones as well as there being sensory involvement via the nervous system. Indeed, it’s been demonstrated there was no increase in insulin nor in appetite following sucralose ingestion[3, 8, 9].

There have also been articles claiming a link between high sucralose intakes with diabetes and heart disease. However, when we look at data we need to be careful, as it may be simply a case of food choice that’s the issue rather than the sweetener itself; for example, people with poor diet choices may be more likely to include low calorie beverages in their diet: this merely demonstrates association and not causality.

There have been some articles claiming an association between sucralose and tumour development, some of which reference the Ramazzini Institute study[10]. There are a number of issues with this study. Firstly, as in the case of the Abou-Donia et al study, this trial was performed on rodents (mice) and not humans: whilst trials on rodents can be useful, they are often quite poor at predicting how humans will react[11].

The second issue refers to the high levels of sucralose that the mice were fed. The US FDA recommends humans do not consume more than 5mg of sucralose per kilogram body weight. The mice receiving the smallest dose of sucralose received 12 times this amount: 60mg of sucralose per kg bodyweight. At very high doses most substances are likely to have a negative effect on your body; even water, for example: consuming 12 times the recommended amount can give rise to water intoxication, with serious adverse reactions; this does not mean clean water is in any way dangerous at typical intakes. At time of writing, no study has found any negative effects from using sucralose when consumed within recommended amounts. There have been well over 100 studies published in peer reviewed articles, some demonstrating that there was no link with tumour in rats at all[2, 12].

Furthermore, whilst the study highlighted that there was a rise in tumour incidence for male mice, female mice actually saw a reduction in cancer. When male and female mice cancer rates are included together, there is essentially no change in the cancer rate at any dosage. Splenda was also fed to the mice throughout their life, including in utero; there may be a specific period during a male mice’s life that cause issues from sucralose consumption at this dose.

Finally, some people point to the fact that this study was published in the peer-reviewed International Journal of Occupational and Environmental Health as evidence of it’s credibility. Peer-reviewed studies are a fantastic tool, and in general lead to a much higher standard throughout the scientific community, but this does not mean that we should assume their mere presence indicates that a study is absolute and without flaw.

Is Sucralose safe?

Sucralose has been demonstrated to be safe for consumption by humans by numerous studies and reports and countries. The adverse press sucralose receives seems primarily to be due to the fact that it is artificial and this term is very much maligned in nutrition. It’s important to note that ‘artificial’ doesn’t always mean bad in the same way as ‘natural’ doesn’t always mean good. A quick internet search will reveal a number of articles and blog posts demonising sucralose and reporting it in a negative manner. These are really only based on poorly designed studies and other articles - most of which have subsequently been discredited - or the fact that naturalistic advocators feel that, because sucralose is artificial, it isn’t good for the body and should be avoided. Too often people latch onto a study and take its results as given ignoring the study design and conflicting factors. The sucralose debate is a clear demonstration of this.

The Japanese and EU safe level of sucralose is 15mg per kg body weight per day[12, 13]. This safe level has been made up with caution in mind and no effects have been reported in levels as much as 1,500mg/kg/day[4]. However, the acceptable daily intake (ADI) in Canada has been set at a recommended 9mg/kg/day[14] and the US ADI is 5mg/kg/day[15].

Alternative sweeteners

There are a large number of other sweeteners permitted in foods. The most obvious one is sugar but a large amount is often needed to meet the required sweetness and sugar has the obvious numerous health disadvantages. There are quite a range of other natural possibilities like fructose, honey, coconut sugar, maple syrup, xylitol and a whole load more. The problem with most of these, is that they are either still effectively sugars or a large amount is required in order to sweeten a product sufficiently.

Other options are artificial sweeteners like aspartame, acesulfame K and saccharin, none of which have any advantage over sucralose. In fact, the taste of sucralose is generally preferred and none of these are without their own health concerns.

The only sweetener which may be a viable alternative to sucralose is the natural sweetener stevia. Stevia is derived from the plant Stevia rebaudiana and steviol glycosides, the active fractions of stevia, are between 150 and 300 times sweeter than sugar. Stevia is very much favoured by naturalistic advocators purely because it’s natural. However, many people feel there is an unfavourable aftertaste in some products where stevia is used as the sole sweetener. Indeed, Coca-Cola have researching this extensively and, although they have used stevia in Coca-Cola Life, they also include a significant amount of sugar in order to achieve a palatable product.


  1. Sims J, et al. The metabolic fate of sucralose in rats. Food Chem Toxicol. 2000;38(2):115-21.
  2. EFSA Panel on Dietetic Products N, et al. Scientific Opinion on the substantiation of health claims related to the sugar replacers xylitol, sorbitol, mannitol, maltitol, lactitol, isomalt, erythritol, D-tagatose, isomaltulose, sucralose and polydextrose and maintenance of tooth mineralisation by decreasing tooth demineralisation (ID 463, 464, 563, 618, 647, 1182, 1591, 2907, 2921, 4300), and reduction of post-prandial glycaemic responses (ID 617, 619, 669, 1590, 1762, 2903, 2908, 2920) pursuant to Article 13(1) of Regulation (EC) No 1924/2006. EFSA Journal. 2011; 9(4):2076.
  3. Brown AW, et al. Short-term consumption of sucralose, a nonnutritive sweetener, is similar to water with regard to select markers of hunger signaling and short-term glucose homeostasis in women. Nutr Res. 2011;31(12):882-8.
  4. Baird IM, et al. Repeated dose study of sucralose tolerance in human subjects. Food Chem Toxicol. 2000;38(2):123–9.
  5. Abou-Donia MB, et al. Splenda alters gut microflora and increases intestinal p-glycoprotein and cytochrome p-450 in male rats. J Tox Environ Health. 2008;71(21):1415-29.
  6. Schiffman SS, Rother KI. Sucralose, A Synthetic Organochlorine Sweetener: Overview of Biological Issues. J Toxicol Environ Health B. 2013;16(7):399–451.
  7. Brusick D, et al. Expert panel report on a study of Splenda in male rats. Reg Toxicol Pharm. 2009;55(1):6-12.
  8. Jing Ma, et al. Effect of the artificial sweetener, sucralose, on gastric emptying and incretin hormone release in healthy subjects. Am J Physiol. 2009;296(4):735-739.
  9. 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;65:508–513.
  10. Soffritti M et al. The Ramazzini Institute: Sucralose administered in feed, beginning prenatally through lifespan, induces hematopoietic neoplasias in male swiss mice. Int J Occ & Environ Health. 2016; 22(1).
  11. Bracken MB. Why animal studies are often poor predictors of human reactions to exposure. Journal of the Royal Society of Medicine. 2009; 102(3):120-2.
  12. The Japan Food Chemical Research Foundation. Safety assessment by JECFA of specified additives. Date Accessed: 19/08/16
  13. European Commission. Opinion of the Scientific Committee on Food on sucralose. 2000.
  14. Diabetes Canada. Sugars and Sweeteners. 2018. Date Accessed: 19/08/16. Available from:
  15. FDA. Food Substances for Direct Addition to Food for Human Consumption. 2018; 21(3).

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