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The most commonly used artificial sweeteners in the Australian food supply are: Name Code number Brand name Acesulphame K Hermesetas® Sunnett® Alitame Aclame® Aspartame Equal® Equal Spoonful® Hermesetas® Nutrasweet® Cyclamate Sucaryl® Neotame Saccharin Sugarella® Sugarine® Sweetex® Sucralose Splenda®. HP XL/ ink cartridges work with: HP OfficeJet Pro dw dw, , , Plus, Premium, Series, , , , , Page yield of /XL: approx. 2, pages black, pages cyan, pages magenta, pages yellow Up to 2x more prints with Original HP ink vs refill cartridges.
A food additive is any substance not normally consumed as a food in itself and not normally used as an ingredient of food, but which is intentionally added to a food to achieve one or more of the technological functions specified in Schedule 5. It or its by-products may remain in the food. Food additives are distinguishable from processing aids see Standard 1.
This standard regulates the use of food additives in the production and processing of food. A food additive may only be added to food where expressly permitted in this standard. Additives can only be added to food in order to achieve an identified technological function according to Good Manufacturing Practice.
Standard 1. Table of Provisions. Schedule 1 Permitted uses of food additives by food type. Schedule 4 Colours permitted to specified levels in processed foods specified in Schedule 1. Schedule 5 Technological functions which may be performed by food additives. This definition of 'processed food' is used to determine some additive how to type copyright logo. Processes such as dividing, parting, severing, boning, mincing, skinning, paring, peeling, grinding, cutting, cleaning, trimming, deep-freezing or freezing, milling or husking, packing or unpacking are not considered to result in a substantial change to the original state of the food.
Unless expressly permitted in this Standard, food additives must not be added to food. The additives listed by name or number in Schedules 1,2,3 and 4 may be added to a food or class of food to perform technological functions provided that:.
The Codex Alimentarius Commission Procedural Manual sets out the following relevant criteria for use in assessing compliance with Good Manufacturing Practice:.
The manner in which a food is intended to be presented eg. Similarly, the type and level of food additives used may affect the way in which a food may be presented. Save where otherwise expressly stated in Schedule 1 and not withstanding any specific level specified in a Schedule to this Standard, intense sweeteners may only be added to food in an amount necessary to replace the sweetness normally provided by sugars or as a flavour enhancer.
In general, the use of intense sweeteners is limited to:. Polyols, isomalt and polydextrose may be considered to be food additives when used as humectants and texturisers. Where these substances constitute a significant part of the final food they would be regarded as a food in their own right rather than food additives.
Polyols, isomalt and polydextrose are not considered to be bulking agents if used in large amounts to replace sugars as they may contribute significantly to the available energy of the food. Some of the permitted combinations of the two preservatives are:. Preservative X Preservative Y Fractions.
Other than by direct addition, an additive may be present in any food as a result of carry-over from an ingredient, provided that the level of the additive in the final food is no greater than would be introduced by the use of the ingredient under proper technological conditions and good manufacturing practice.
In clause 7, the ingredient can itself be a food additive. The additive must be permitted to be present in the ingredient and must not be present in any greater quantity than permitted.
A food intended for use in the preparation of another food may contain any or all of the additives in a quantity permitted in the final food. The addition of a garnish to a food does not render that food a mixed food for the purposes of this Standard. Examples what are sweeteners 951 and 950 the addition of how to run remote desktop on mac garnish to a food include lemon slice to fish or pepper to steak to make pepper steak.
A reference to a colour listed in Schedules 1, 3 and 4 of this Standard includes a reference to the aluminium and calcium lakes prepared from that colour. Permitted synthetic flavourings, for the purposes of this Standard, are those synthetic flavourings listed in at least one of the following publications:. Editorial note:. INS Number. Additive Name. Max level. Additives in Schedule 2 may be present in processed foods as a result of use in accordance with GMP except where expressly prohibited in this schedule.
Colours in Schedule 3 may be present in processed foods as a result of use in accordance with GMP except where expressly prohibited in this schedule. Preparations of food additives. Does not apply to preparations of colours or flavours.
Preparations of colours and flavours only. Sorbic acid and sodium, potassium and calcium sorbates. Benzoic acid and sodium, potassium and calcium benzoates. Propyl p -hydroxybenzoate propylparaben. Methyl p what does a northern spotted owl eat methylparaben. Sulphur dioxide and sodium and potassium sulphites. Ascorbyl palmitate.
Tocopherols concentrate mixed. Tocopherol, d-alpha- concentrate. Synthetic gamma-tocopherol. Synthetic delta-tocopherol. Propyl gallate. Octyl gallate. Dodecyl gallate. Tertiary butylhydroquinone. Butylated hydroxyanisole. Calcium disodium EDTA. Sodium aluminium phosphate. Benzyl alcohol. Ethyl acetate. Glycerol diacetate. Glyceryl monoacetate. Isopropyl alcohol. Triethyl citrate. Liquid milk and liquid milk based drinks.
Liquid milk including buttermilk. Additives in Schedule 2. UHT goat milk only. Annatto extracts. Acesulphame potassium. Fermented and rennetted milk products.
Fermented milk and rennetted milk. Cream and cream products. Cream, reduced cream and light cream. UHT creams and creams receiving equivalent or greater heat treatments only. Cream products flavoured, whipped, thickened, sour cream etc. Polyglycerol esters of fatty acids. Magnesium phosphates. Polyoxyethylene 40 stearate. Sodium lactylates.
Magnesium oxide. Bone phosphate. Potassium aluminium silicate. Sulphur dioxide and sodium and potassium sulphates. Pimaricin natamycin. Nitrates potassium and sodium salts. Phosphoric what are sweeteners 951 and 950. Potassium silicate. Butylated hydroxytoluene. Polyglycerol esters of interesterified ricinoleic acids.
Oil emulsions water in oil. Additives must not be present in butter unless expressly permitted below. Potassium chloride. Sodium propionate. How to use a petzl shunt propionate. Unprocessed fruits and vegetables.
Untreated fruits and vegetables. Surface treated fruits and vegetables.
Effects of intensive sweeteners on the gut microbiota. Intensive sweeteners have negligible caloric content and high-power sweetening and are used in low quantities in foods. All of them have been classified in synthetic and natural sweeteners. Their structures and ADI, as well as their main biological effects, are summarized in Table 1. Sep 30, · 4 Requirements for use of intense sweeteners. 5 Maximum permitted levels of additives. 6 Additives performing the same function Acesulphame potassium. mg/kg. Alitame. mg/kg. Fermented and rennetted milk products Aspartame. GMP. note - duplication of schedule 2. Sucralose. GMP. note - duplication of. “Coke Zero and Diet Coke are actually very similar. Both are low calorie drinks and have exactly the same ingredients – carbonated purified water, colour (caramel d), food acids ( and ), flavour, artificial sweeteners aspartame () and acesulphame potassium (
The consumption of sugar-free foods is growing because of their low-calorie content and the health concerns about products with high sugar content. Sweeteners that are frequently several hundred thousand times sweeter than sucrose are being consumed as sugar substitutes.
Although nonnutritive sweeteners NNSs are considered safe and well tolerated, their effects on glucose intolerance, the activation of sweet taste receptors, and alterations to the composition of the intestinal microbiota are controversial.
This review critically discusses the evidence supporting the effects of NNSs, both synthetic sweeteners acesulfame K, aspartame, cyclamate, saccharin, neotame, advantame, and sucralose and natural sweeteners NSs; thaumatin, steviol glucosides, monellin, neohesperidin dihydrochalcone, and glycyrrhizin and nutritive sweeteners polyols or sugar alcohols on the composition of microbiota in the human gut. So far, only saccharin and sucralose NNSs and stevia NS change the composition of the gut microbiota.
By definition, a prebiotic is a nondigestible food ingredient, but some polyols can be absorbed, at least partially, in the small intestine by passive diffusion: however, a number of them, such as isomalt, maltitol, lactitol, and xylitol, can reach the large bowel and increase the numbers of bifidobacteria in humans. Further research on the effects of sweeteners on the composition of the human gut microbiome is necessary.
The consumption of sugars, mainly as sucrose and glucose-fructose syrups, has dramatically increased worldwide and growing concerns about their adverse effects on health and metabolic diseases, such as metabolic syndrome, cardiovascular diseases, and type 2 diabetes T2D , have motivated people to reduce the consumption of free sugars.
Sweeteners are sugar substitutes that mimic the sweet taste of sugar but have a negligible impact on energy intake 1 , 2. The sweetness of sweeteners is measured in relation to the reference sugar sucrose. Biologically, the perception of sweetness occurs through the receptors on the taste buds, which are coupled to G proteins [taste receptor types 1 and 2 T1R1 and T1R2, respectively ] that form part of the C class of proteins 3.
Nonnutritive sweeteners NNSs are defined as sweetening agents that have a higher sweetening intensity and lower calorie content per gram compared with caloric or nutritive sweeteners such as sucrose or corn syrup. NNSs can be of synthetic or natural origin, the latter being increasingly consumed 4 , 5. Low-calorie sweeteners LCSs , such as polyols or sugar alcohols and other new sugars, are low-digestible carbohydrates derived from the hydrogenation of their sugar or syrup sources.
Sugar alcohols are slightly lower in calories than sugar and do not promote tooth decay or cause a sudden increase in blood glucose 6. Both NNSs and LCSs are consumed not only by people with diabetes but also by the general population, because they are used as ingredients in many reduced-calorie foods such as soft drinks, dairy products, powdered drink mixes, baked goods, desserts, candy, chocolates, puddings, canned foods, jams and jellies, and confectionery chewing gums.
In addition, they can be used as tabletop sweeteners at home, in cafeterias, and in restaurants 6. The US FDA approval process for sweeteners includes determining the probable intake amounts, the cumulative effects of the sweetener from all of its uses, and toxicology studies in animals. To date, the FDA has approved 6 high-intensity artificial sweeteners for foods and drinks: acesulfame potassium acesulfame K , aspartame, neotame, saccharin, sucralose, and advantame.
In addition, 3 NNSs of natural origin—steviol glycosides, thaumatin, and luo han guo fruit extracts—have been approved by the FDA 6. The EU EFSA has approved 11 NNSs for human consumption: acesulfame K E , advantame E , aspartame E , aspartame-acesulfame salt E , cyclamic acid and its sodium and calcium salts E , neohesperidin dihydrochalcone E , neotame E , saccharin E , steviol glycosides E, including 10 different glycosides , sucralose E , and thaumatin E 7. Food-use—approved polyols are low-calorie carbohydrates with a sweet taste used, volume-for-volume, as a substitute for sucrose and other free sugars.
They include erythritol, hydrogenated starch hydrolysates sometimes listed as maltitol syrup, hydrogenated glucose syrup, polyglycitol, polyglucitol, or simply HSH , isomalt, lactitol, maltitol, mannitol, sorbitol, and xylitol.
The approved LCSs in the EU include the following: sorbitol and sorbitol syrup E , mannitol E , isomalt E , polyglycitol syrup E , maltitol and maltitol syrup E , lactitol E , xylitol E , and erythritol E 7. The consumption of NNSs, mainly in diet sodas, has been related to an increased risk of obesity, metabolic syndrome, and T2D 8—12 , although some studies did not find any association 13 , The consumption of typically used nonnutritive artificial sweetener formulations drives the development of glucose intolerance through the induction of compositional and functional alterations to the intestinal microbiota In contrast, the consumption of NNSs reduces blood glucose, which is attributed to the lower carbohydrate load rather than the activation of sweet taste receptors In some people, the excessive consumption of polyols may cause gastrointestinal symptoms such as gas or laxative effects, similar to the gastrointestinal reaction to beans and certain high-fiber foods.
Such symptoms depend on an individual's sensitivity and the other foods eaten at the same time Intestinal microbial communities play a significant role in human health and disease; indeed, the intestinal microbiome is involved in metabolism, immunity, growth, and the fermentation of undigested carbohydrates More importantly, the gut microbiota cooperates with the immune system, providing signals to promote the maturation of immune cells and the induction of susceptibility to many pathophysiologic conditions The composition and function of the microbiome are modulated and can be rapidly altered by diet However, there are many gaps in the evidence related to the health effects of NNSs and LCSs in both healthy and nonhealthy populations.
Intensive sweeteners have negligible caloric content and high-power sweetening and are used in low quantities in foods. All of them have been classified in synthetic and natural sweeteners 5. Their structures and ADI, as well as their main biological effects, are summarized in Table 1. Structure, ADI, and biological effects of natural and synthetic sweeteners 1.
Acesulfame is an acidic cyclic sulfonamide and acesulfame K E is the potassium salt of acesulfame. Acesulfame K decreases glucose fermentation by the cecal microbiota in Cara rats, suggesting that sweeteners might affect glucose transport systems The effects of acesulfame K were not associated with gut microbial functional capability In contrast, Bian et al.
Bacteroides were highly increased in acesulfame K—treated male mice and significant changes in Anaerostipes and Sutterella populations occurred as well.
Conversely, in female mice, acesulfame K treatment decreased the relative abundance of Lactobacillus and Clostridium. Those changes in the populations of gut microbiota after the consumption of acesulfame K indicate sex-specific effects With regard to human consumption, the Uebanso et al.
Indeed, this work might be physiologically irrelevant The metabolism and fate of aspartame are dominated by presystemic hydrolysis to the constituent parts, with little or no parent compound entering the general circulation. According to EU regulation no. A mg dose of aspartame did not affect the peak insulin concentrations in subjects with or without diabetes but did cause a decrease in plasma glucose concentrations Tordoff and Alleva 27 compared the consumption of aspartame and high-fructose corn syrup and concluded that aspartame reduces sugar intake.
Although we have a huge quantity of information with regard to aspartame safety in humans, few of those studies focused on the effects of aspartame intake on the composition of gut microbiota. In rats, the impact of chronic low-dose aspartame consumption on anthropometric, metabolic, and microbial variables was tested in a diet-induced obesity model. Aspartame consumption increased the fasting glucose concentrations in both the standard feed pellet diet and high-fat groups independent of body composition.
A metabolomics analysis showed that aspartame was rapidly metabolized and related to SCFA production, especially propionate production. Changes in the microbial composition were observed in animals that received aspartame; the total bacteria and abundance of Enterobacteriaceae and Clostridium leptum increased In addition, mice treated with aspartame for 11 wk developed glucose intolerance, although analyses of the microbiota did not show significant differences between the groups To our knowledge, there are no data on the potential influences of aspartame on the human gut microbiome.
It is hard to understand how aspartame influences the gut microbiota because this NNS is rapidly hydrolyzed in the small intestine. Upon ingestion, aspartame breaks down into residual components, including aspartic acid, phenylalanine, and methanol and their components, which are readily absorbed so that they do not reach the large bowel Neotame E is an artificial sweetener that is between and 13, times sweeter than sucrose with a structure close to that of aspartame [i.
The suggested ADI is 0. Neotame is moderately heat stable, extremely potent, rapidly metabolized, completely eliminated, and does not appear to accumulate in the body. Mice and other test animals fed neotame did not show adverse physical symptoms, water consumption, or clinical pathology evaluations and there were no reports of morbidity, mortality, organ toxicity, or macroscopic or microscopic postmortem findings 31— Neither sweetener has been evaluated in animals or in humans because only trace amounts of advantame or neotame are needed to sweeten foods.
The amount of methanol derived from the intestinal hydrolysis of neotame is much lower than that found in common foods; therefore, it is improbable that either neotame or advantame would have any influence on the gut microbiota.
This was because of the detection of bladder tumors in rats fed a cyclamate-saccharin mixture supplemented with cyclohexylamine, a metabolite of cyclamate that is more toxic than cyclamate alone 35 , However, these studies were severely criticized because of their designs and doses 37 and cyclamate is being reevaluated. The first finding of microbiota changes caused by cyclamate was reported in the study by Drasar et al.
The authors observed that the conversion of cyclamate to cyclohexylamine in rats does not occur after either parenteral administration of cyclamate or with incubations of cyclamate with the liver, spleen, kidney, or blood preparations. The principal hypothesis was that cyclohexylamine formation occurred solely in the gut as the result of microorganism metabolism In , Mallett et al. They found a maximum formation of cycloheximide at 8 wk and increased levels of sulfamatase activity in the fecal content.
The authors did not find any taxonomic changes in the fecal microbiota cultured in an in vitro system after the administration of cyclamate. The presence of cyclamate decreased the fermentation of glucose by the microbiota in Cara rats Cyclamate increases the bacterial sulfatase activity in the intestine To our knowledge, there are no available data on the effects of cyclamate on gut microbiota in humans.
A range of food and beverages are sweetened by saccharin E , which is considered safe despite controversial debate about its potential carcinogenicity. However, studies indicate that the consumption of saccharin might perturb the gut microbiota. The effect of 7. The presence of saccharin did not alter the total numbers of anaerobic microbes but resulted in the elimination of a specific anaerobic group of microbes from the cecal contents Saccharin administration inhibited the growth of 6 bacterial strains 3 Lactobacillus species and 3 Escherichia coli strains isolated from the small intestinal contents in rats that received a 2.
Saccharin inhibited the fermentation of glucose by the microbiota from Cara rats Pyrosequencing studies in animals showed that the addition of saccharin plus neohesperidin dihydrochalcone increases the abundance of the Lactobacillus cecal population and increases intraluminal lactic acid concentrations The deleterious metabolic effects of saccharin in animals were abrogated by antibiotic treatment and were fully transferrable to germ-free mice upon microbiota transplantation.
In addition, the altered metabolic pathways were linked with glucose tolerance and dysbiosis in healthy human subjects. In mice fed saccharin, Akkermansia muciniphila , a commensal bacterium that exhibits probiotic properties, was underrepresented Since the study by Suez et al. Sweeteners are often used to encourage the consumption of agents such as ethanol and nicotine in laboratory studies that use rodents. Labrecque et al. Saccharin reduced Clostridium numbers, even though the total amounts of ethanol consumed were the same for the 2 groups Inflammation is frequently associated with disruptions to the gut microbiota.
Mice treated with 0. In addition, altered gut bacterial genera were associated with saccharin-induced liver inflammation. These changes in the intestinal microbiota were observed in Ruminococcus , Adlercreutzia , Dorea , Corynebacterium , Roseburia , and Turicibacter Early studies suggest that artificial sweeteners maintain plasma glucose and peak insulin concentrations without affecting the gut microbiota.
However, more recent animal and human studies showed specific changes in the intestinal microbiota related to alterations in the metabolic pathways linked to glucose tolerance and dysbiosis in human subjects, especially with the ingestion of saccharin Figure 1. Effects of artificial sweeteners and saccharin on gut microbiota.
Animal studies have reported specific shifts in the intestinal microbiota related to alterations in the metabolic pathways linked to glucose tolerance after ingestion of saccharin. The first study that evaluated sucralose on the intestinal microbiota was performed in with the use of fecal samples from Sprague-Dawley rats that received the sweetener for 12 wk.