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All You Need to Know about Sugar and Sugar Substitutes

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The amount of sugar we consume in foods and beverages would likely astound you because so much of it is hidden in different names.  There are many different variations of sugar that can be encountered on labels which are not easy for an untrained eye to recognize, so it’s easy to consume more sugar than recommended.

For a touch of sweetness in food and drink, there are many alternatives to regular table sugar available.  Many people turn to sugar substitutes to reduce their sugar consumption, but how much do we really know about these synthetic sweeteners?

What are some of these variations of standard sugar, and what are some of the sugar substitutes?  Below we explore the many different ways sugar is represented and the various sugar substitutes while uncovering the mechanisms of how the body processes each one and their side effects.

How the Body Processes Food into Fuel

The body needs glucose for energy in nearly every cell, especially to fuel muscles and the brain (1)(2).

The process after you eat food of any kind involves the food being digested and broken down into smaller units.  In the case of ingesting carbohydrates or table sugar, the body breaks it down into glucose, which is released directly into the bloodstream.  From the bloodstream, it travels to the muscle and organ tissue cells where it can be used as energy.

When the body senses a rise in sugar levels in the blood, specialized cells in the pancreas start to work.  These pancreatic beta cells release a hormone called insulin.  Insulin is the great balancer in the body between blood sugar levels being too low (hypoglycemia) or too high (hyperglycemia).  The beta cells are stimulated to release insulin into the bloodstream, which then signals the cells to open up and let the sugar (glucose) enter, so the cells can use the sugar for energy (3).

If too much glucose is in the bloodstream, insulin will signal the liver to begin storing the extra glucose there.  The extra glucose remains stored in the liver until a time when the levels fall, and it needs to be released from storage to increase blood glucose levels.  Balanced insulin levels ensure that the levels of glucose in the body are as constant as possible.

The body uses glucose to make the building blocks of cellular energy, ATP (adenosine triphosphate), and a citrate molecule.  After the body has produced enough ATP,  a signal is sent to the liver which tells it how much glucose should be stored, based on how many energy molecules have been created. Some of the unused glucose will then deposit itself as fat within subcutaneous tissues (4).

What is sugar?

As a substance, sugar is granular and ranges in color from brown, to golden brown, to white.  It is commonly harvested from either beets or sugarcane.  Sugar is a complicated molecule; and unfortunately, it is very easy to confuse it with different molecules that are commonly grouped together as “sugars.” All sugars are forms of carbohydrates.

You may have heard of sugar being called “glucose,” as the common phrase “blood glucose” is commonly interchanged with “blood sugar.” This may lead you to infer that the granular sugar on your tabletop is glucose–however, table sugar is actually called sucrose!  First, we’ll explore the differences between these two (5).

Monosaccharides

  • Are called simple sugars
  • Consist of one “sugar” molecule
  • Glucose, fructose, and galactose

Glucose vs. Sucrose

Glucose is a “simple sugar” because it is composed of a single molecule (2).  Simple sugars are called monosaccharides (mono=one molecule, and saccharides=sugars).  The simple sugars (monosaccharides) consist of glucose, fructose, and galactose (6).

The classification of a sugar being “simple” or “complex” is based on the number of molecules it contains.  Once you get beyond simple sugars (or monosaccharides), the sugar is classified as complex.

There are 3 types of complex sugars (called disaccharides, oligosaccharides, and polysaccharides). The disaccharides consist of 2 sugar molecules bound together and include sucrose, maltose, and lactose.  The oligosaccharides contain 3 to 10 sugar molecules bound together and include substances called fructo-oligosaccharides and galactooligosaccharides.  Polysaccharides contain more than 10 sugar molecules bound to one another and include starch, cellulose, and chitin (6)(7)(8).

After ingestion, all carbohydrates (including starchy grains and vegetables) and complex sugars are broken down into glucose.  Glucose is the preferred form of sugar the body uses.  The body breaks down all carbohydrates into glucose because it recognizes all glucose as the same.  It does not differentiate between naturally occurring glucose or added glucose (2).

Though they share the same common name of “sugars,” sucrose and glucose are different molecules (5). Sucrose is a complex sugar called a disaccharide (di=two, saccharide=sugar).  It is composed of two simple sugar molecules which have joined together (2). Sucrose is found naturally occurring in fruits and vegetables.

The two molecules of sucrose consist of equal parts of the simple sugar glucose and the simple sugar fructose. When the body consumes sucrose, it is broken down into its simple sugar parts, so that glucose and fructose are both released in the bloodstream. While the body can readily use and consume the glucose, the fructose can only be broken down by the liver cells (2)(1).

Summary

The notion that the sugar on your table is the same sugar as glucose, or that all “sugars” are the same, is inaccurate. Once you’ve grasped the concept that the word “sugar” is colloquially used to refer to many different molecules that are chemically separate from one another, it becomes easier to understand how each type of “sugar” causes a different reaction in the body.

Fructose vs. Glucose

Fructose is one of the easiest types of the simple sugars to name because it is on so many labels.  Usually, it is accompanied by the words “high-fructose corn syrup.”  The process and differentiation of high-fructose corn syrup will be explained below, but let’s look at what separates fructose from one of the other simple sugars, glucose.

Because you’ll find sucrose (which is glucose + fructose) in fruits and vegetables, you will also find fructose in many fruits and vegetables.  Of all the naturally occurring carbohydrates, fructose is the sweetest.  It is due to its sweetness that it is used so widely, and we are most familiar it.  Fructose is approximately 1.73 times sweeter than sucrose (9).

Fructose is sent to the liver for metabolism, where it can undergo one of three processes.  It can either be released as glucose into the bloodstream, or as a lactate, or as fatty acids (4).

Some of the fructose that is ingested will be converted into glucose.  The metabolism of fructose skips a vital, rate-limiting conversion step that is very important to processing glucose, wreaking havoc on the body.  Missing the rate-limiting conversion step means that fructose doesn’t activate the secretion of insulin.  Therefore, when the insulin pathway isn’t activated after consuming fructose, the body doesn’t realize that there is a large amount of sugar waiting around to be processed.  The body doesn’t sense that there is adequate glucose in the blood; and because it needs glucose to make ATP for cellular energy, it continues to process fructose into glucose.  This creates an abnormally high level of glucose in the bloodstream which does not have the benefit of the release of insulin to allow the glucose to enter the cells.

Problematically, the body also does not get the signal that the cells have gotten enough energy yet, because it is not using the same signals that glucose metabolism would normally use.  Normally, the signals would indicate that there is more ATP for cellular energy available, signaling the body to limit the conversion of fructose to glucose because it senses that enough ATP has been created.  This would signal the body to start storing the fructose, which has been converted into glucose, in the liver.

Without this pathway and rate-limiting step, the liver metabolism continues on unchecked and the excess fructose, now converted into glucose, has no run-off pathway.  Instead, excessive fructose, which has been converted into glucose, is stored as fat, leading to obesity (4).

The Problem with Excessive Fructose Intake

Due to the relationship between the liver and fructose, fructose presents some unique complications to the body when it is ingested in amounts which exceed recommended daily allowances.  One of the end-products of fructose metabolism in the liver is triglycerides (a fat molecule).  Triglycerides contribute to the fat deposits which line artery walls and cause plaques, as well as accumulating in the cells of the liver and damaging the function of the liver.

Along with triglycerides, excessive fructose metabolism can release free radicals and uric acid.  The free radicals (also referred to as reactive oxygen species) are free-roaming agents of oxidative damage within the body which can wreak havoc on enzymes, cell structures, and genes.  Uric acid can block the body’s ability to produce nitric oxide which is a protective substance that prevents the walls of the arteries from becoming damaged (1).

Another complication of fructose metabolism is that excessive consumption (which is not hard to accidentally achieve because of its over-use and hidden names on labels) can lead to a metabolic condition called insulin resistance.  Shockingly, it only takes a mere 6 days of excessive fructose consumption to cause insulin resistance!  A study was conducted in healthy subjects who received a quarter of their daily calorie consumption in the form of Kool-Aid—an amount which you may think is unrealistic, but we know many people consume excessive amounts of calories through sweetened beverages in this exact way.  The two groups were separated and received Kool-Aid sweetened with glucose or fructose.  Within only 8 weeks, the group receiving the fructose-sweetened beverage had become so insulin resistant that these previously healthy volunteers were now clinically diagnosed with pre-diabetes (10).

Fructose is about 20 times more likely to cause insulin resistance issues versus glucose.  It’s mainly the metabolism of fructose by the liver that causes all the problems.  Whereas glucose can be metabolized and used by all the tissues of the body (say, the entire body weight of an average adult which is generally over 150 pounds), fructose can only be metabolized by the single organ of the liver, which generally weighs less than 5 pounds.

Additionally, because there is no pathway for excessive fructose in the body (unlike glucose which can be stored in the liver), any excess is deposited in the fat.

Again, the notion that all sugar is equal–when it is actually very different– explains why there is a collective misunderstanding about sugars and carbohydrates.  Some people and cultures can eat vast quantities of carbohydrates and grains and not experience any obesity problems; whereas a culture, heavily influenced by the addition of fructose and high-fructose corn syrup in their sodas and beverages, is likely to experience obesity (10).

What is high-fructose corn syrup?

High-fructose corn syrup (HFCS) is an artificial sweetener agent made from corn.  The corn is first processed into corn starch and then liquified into corn syrup.  At this stage, because it is pure carbohydrates, it is also pure glucose.  Unfortunately, pure glucose is not very sweet, so the producers of HFCS use enzymes to catalyze the conversion of some of the glucose to fructose (11). HFCS is then composed of 55% fructose and 45% glucose (2).

If you’ll recall, sucrose (table sugar) is equal parts glucose and fructose, which make up the end-product mixture of HFCS.  The great difference between the two is that the formulation and manipulation involved in making high-fructose corn syrup prevents glucose and fructose from becoming bonded to one another.  Therefore, the glucose and fructose that are present in HFCS consists of free molecules of each (11).

Galactose, the last simple sugar

Galactose is structurally similar to glucose except in its hydroxyl group’s position.  Galactose is the simple sugar that contributes to a complex sugar, lactose.  By itself, galactose is only ever found in very small, trace amounts in some seeds and pulses, and within dairy products as a component of lactose (12).

Disaccharides

  • Sucrose, Lactose, Maltose

Lactose

The primary dietary source of galactose is via lactose.  Lactose is a disaccharide composed of one glucose molecule and one molecule of galactose.  Lactose can only be found in milk or dairy products.  Human milk contains the most lactose (7.2 g per 100 g), while cows’ milk and goats’ milk contain concentrations similar to one another (around 4.7 g per 100 g of milk) (12).

It is possible to find lactose in non-dairy products because it is sometimes used to produce a lactose hydrolysate syrup that is used for a sweetener in confectionaries, biscuits, and some dairy desserts (12).

We’ve looked into sucrose and lactose above as two of the three disaccharides.  The final disaccharide is maltose.

Maltose

Maltose is composed of two glucose molecules bound together, often called “malt sugar.”  It is called malt sugar because it is formed after enzymes break down starches.  This process occurs naturally in seeds which are germinating.  The seeds of barley are often soaked in water in order to germinate and produce malt, which is then used for brewing, malt vinegar, malted milk, confections (Whoppers and other malt-flavored candy), flavored malt drinks (Ovaltine), and some baked goods.  Maltose is the type of carbohydrate found in molasses (13).

Malt is naturally sweet; depending on the concentration, it can be 30-60% of the sweetness of table sugar (13).

Sugar Substitutes

Unlike sugars which provide the body with carbohydrates for usable energy, sugar substitutes belong to a class of substances called “nonnutritive sweeteners.”  They are also often called high-intensity sweeteners because they are concentrated and usually much sweeter than sugar, requiring lesser quantities to achieve a sweetened taste.

They do not provide any nutrients because they do not contain any protein, fats, or carbohydrates.  Since they do not contain any usable energy for the body, they contain either few or no calories.  They can be derived from sugar, plants, or herbs.

There are eight nonnutritive sweeteners that have been approved for use by the U.S. FDA which we focus on below (aspartame, saccharin, acesulfame potassium, sucralose, stevia, monk fruit, advantame, and neotame).  [Advantame, neotame, and the sugar alcohol family will be covered in a subsequent article.]   

From saccharin to aspartame, sucralose, acesulfame potassium, stevia, reb-A, monk fruit, and the family of sugar alcohols (erythritol, xylitol, maltitol, mannitol, sorbitol, and lactitol):  there are probably some familiar artificial sweeteners you recognize from this list, and most likely a few you’ve never heard of.

Below, we’ll go over the most common and popular sugar substitutes, their origins, how the body metabolizes them, their side effects, and which of them are good choices.

Saccharin

Sugar substitutes started with the discovery of saccharin.  Saccharin was actually discovered in 1879 when scientists stumbled upon this coal-tar derivative—but you most likely know it by its trade name “Sweet’N Low ®,” “Necta Sweet ®,” or “Sweet Twin ®.”  It is 300 times sweeter than sugar and has had one of the most tumultuous histories of approval and disapproval in the realm of non-nutritive sugar substitutes (14)(15)(16).

History

After the discovery of saccharin at Johns Hopkins University, it was widely used to sweeten canned foods.  As of 1907, it was approved for additions to food; but just five years later, its status was changed to banned.  As World War I raged and sugar became scarce, saccharin was deemed safe again.  Its use and popularity rose until the 1950’s when it was becoming evident that there were potential adverse effects.

This change of heart was induced by the marketing of yet another sugar substitute, cyclamate.  Cyclamate was another accidental discovery, this time by Abbot Laboratories.  Though it was isolated chemically in 1937 when research was being conducted on fever reducing drugs, it wasn’t until 1951 that it received FDA approval for addition to foods.

Cyclamate was the first diet soda sweetener, introduced as “No-cal” in 1953 by Kirsch Beverages Corp.  It was often used in conjunction with saccharin in everything from toothpaste, mouthwash, lipstick, cereal, bacon, baked goods, and canned goods.

With two competing sugar substitutes on the market, more research was warranted.  The use of cyclamate continued unchecked until testing was performed on cyclamate and saccharin.  Cyclamate was linked to bladder tumors in rats.  In 1969, cyclamate was banned (14).

The official ruling on saccharin’s safety wavered over the next few decades.  It was necessary for all products containing saccharin to have a warning label in 1977; but the label was removed in 2000 because more information about the rodent study came to light.  Researchers discovered that it was a unique attribute of rat physiology that caused saccharin to form microcrystals in the bladder, which was not manifested in humans.

As of 2010, the EPA has ruled that saccharin is no longer considered potentially hazardous.  Despite its current favor, many people choose to avoid saccharin because of the stigma associated from its early days (17).

Mode of Action

Saccharin (1,2-benzisothiazole) is a petroleum derivative in the family of aromatic homomoncyclic compounds.  In high concentrations, it has a bitter and metallic aftertaste (18)(19).  It is heat stable, which is not a property shared by some of its successors.

Scientists believe the reason why saccharin seems sweet to taste buds is because of its molecular shape which may fit into the human taste bud.

After ingestion, saccharin is not metabolized nor absorbed.  It is a completely non-nutritive substance, but it is capable of triggering a release of insulin because of its taste due to “cephalic phase insulin release.”

Common products

Saccharin can be found in a variety of products from chewing gum, salad dressings, baked goods, canned fruit, jams, and dessert toppings.  It is also found in non-food products such as cosmetics, pharmaceutical medications, and vitamins (19).

Safety and Side Effects

  • Saccharin can raise blood glucose levels

A study conducted in mice found that after being fed for 11 weeks with an artificial sweetener (either saccharin, aspartame, or sucralose), their blood sugar levels were surprisingly high (20)(21).

A study of the same sort followed healthy adults who exceeded the recommended daily allowance of saccharin for 5 days and found that 4 of the 7 participants also had unusually high blood sugar levels after the experiment (20).

  • Saccharin may change gut bacteria

The same study which found unusually high blood glucose levels in healthy adults also found that the same 4 participants whose blood sugar was elevated after saccharin consumption also had changes in their gut bacteria (20).

  • Saccharin passes through breastmilk

Saccharin is the only nonnutritive sweetener which is viewed as unsafe during lactation.  It can also be detected in breast milk after ingestion by the mother (22).

The ban on saccharin that was imposed by several different countries, including the U.S. and Canada, may have lifted, but saccharin is still considered the worst of all the artificial sweeteners due to its associated reputation.

If you are the slightest bit concerned about consuming saccharin, there are many other, better, and safer choices that can take the place of sugar which you can enjoy guilt-free.  If you are strict about your saccharin avoidance, don’t forget about checking the labels of your cosmetics, vitamins, medications, chewing gum, and other unlikely areas in which saccharin may still be used.

Aspartame

On the heels of saccharin came aspartame.  You may know it as Equal ®, Nutrasweet ®, or Sugar Twin ® (or in the European Union, it is known as E951).  It is 180 times sweeter than table sugar (23).

[Derivatives of aspartame (neotame and advantame) will be covered in a separate article.]

History

Aspartame was discovered in 1965 after a chemist, working on an anti-ulcer medication, combined two amino acids:  phenylalanine and aspartic acid.  After tasting it, the chemist James M. Schlatter realized it tasted sweet.  Whereas saccharin went straight to the public without enough testing or research, aspartame enjoyed more time being tested before going public.  It was available for manufacturing as of 1982.

Since cyclamate was banned and saccharin was the only sugar substitute available until this point, the inception of aspartame was viewed as a gold mine in which the lucrative field of sugar substitutes could offer an opportunity to de-monopolize the market in which saccharin was king (14).

After the FDA approval for aspartame came three regulations related to labeling.  The unique composition of aspartame containing phenylalanine poses a health risk for people who have to be very aware of their intake of this amino acid.  All products containing aspartame now must bear the statement:  “PHENYLKETONURICS: CONTAINS PHENYLALANINE.”

The second regulation stated that when aspartame was packaged as a tabletop sweetener, it must contain a warning level not to use aspartame in cooking or baking because aspartame is not heat stable (unlike saccharin) and breaks down.  Aspartame, when broken down by heat, loses its sweet taste.

The third regulation was that aspartame must be classified as a “special dietary use” substance, meaning that from now on it had to comply with the special dietary foods’ regulations under the FDA (14).

Mode of Action

Aspartame (aspartyl-phenylalanine-1-methyl ester) is a methyl ester of the amino acids: phenylalanine and aspartic acid (24).

After ingestion, it breaks down into those same constituents.  About 40% of aspartame breaks down into aspartic acid.  It is metabolized and absorbed quickly in the body.  The proteins in foods that contain aspartic acid do not metabolize as quickly.  Due to its fast metabolization, aspartame can quickly cause a spike in the levels of aspartate present in blood plasma.  Aspartic acid, by nature, is an excitotoxin, and excessive amounts of excitotoxins can cause neurotoxicity and damage to the brain (24).

Aspartame contains methanol, which in and of itself is usually found bound to pectin in fruits and does not cause any complications within the body.  In the case of aspartame, however, this methanol is bound so weakly to the phenylalanine molecule that it breaks the bond and causes the methanol molecule to circulate freely.  This is referred to as a “free methanol.”  The bonds can be broken by heat over 85 degrees Fahrenheit in products containing aspartame; meaning that by the time your diet soda or aspartame-containing product reaches you, it has already endured a significant time in warehouse or truck in these conditions.  This means that the methanol is already floating freely before the product even reaches you (25).

This free methanol molecule is converted into formaldehyde in the body and can cross the blood-brain barrier.  In other animals, except humans, formaldehyde can be broken down into a benign substance called formic acid.  However, humans lack an enzyme which catalyzes the conversion, rendering the formaldehyde intact in the body (25).

Common products

Aspartame is found in carbonated beverages and their concentrated syrups, instant coffee, tea, puddings, gelatins, fillings, dairy products, as a tabletop sweetener, in dry breakfast cereals, and in chewing gum (16).

Safety and Side Effects

  • Potential Cancer Risk

It has been implicated, like all artificial sweeteners, that aspartame may be carcinogenic.  The most comprehensive study noting its ability to increase certain types of cancer in rats was associated with very high doses (the amount equal to about 8-2,083 cans of diet soda per day), and the study was scrutinized and reviewed by the FDA, the U.K.’s Food Standards Agency, and the European Food Safety Authority for interpretation, analysis, and quality reviews.  The study was disregarded after the investigation.

In human studies regarding aspartame and cancer, there were some positive correlations between increased risk of cancers–but the results were mixed.  One study from 1996 linked artificial sweetener use to the increase of brain tumors; but when the study was scrutinized by the National Cancer Institute, they found that brain tumor increase began 8 years before aspartame was accessible to the public.  They also found the group was people 70 years old and older who did not have any frequent exposure to artificial sweeteners (27).

Aspartame was studied on its own in 2012 and was associated with an increased risk of leukemia, lymphoma, and multiple myeloma in men only.  The discrepancy between disease risk and gender lead to the study being debunked and claims that such results could be simply based on chance.  The scientists working on the study also agreed that their case was not strong enough, and they issued an official apology (28).

  • Phenylketonuria Precautions

The condition which prompted the warning label to be included on all aspartame-containing products stating “PHENYLKETONURICS: CONTAINS PHENYLALANINE” is for people who have PKU (Phenylketonuria).

People with PKU are unable to metabolize phenylalanine, which makes consuming aspartame toxic (29).

  • Tardive dyskinesia Precautions

Tardive dyskinesia is a condition of uncontrolled muscle movements which may be caused by some medications used to treat schizophrenia.  For people who are schizophrenic and/or taking medications, ingesting the phenylalanine in aspartame may induce tardive dyskinesia (30).

  • Formaldehyde Concerns

If you recall, the free methanol from the disrupted bond in aspartame subsequently converts to formaldehyde in the body.

Methanol on its own is considered carcinogenic, and formaldehyde (as the main ingredient in embalming fluid) is also carcinogenic (25).

Despite the chemical implications of aspartame, it is viewed safe for the general population if you do not have PKU.  The FDA reports that over 100 studies have confirmed its safety as a food additive.

Again, if you are the slightest bit concerned about consuming aspartame, there are many other, better, and safer choices that can take the place of sugar.

Acesulfame Potassium

Acesulfame Potassium is often labeled directly as itself or under the names Sunett® and Sweet One®.  You may also hear it referred to as Ace-K (16).     It is 200 times sweeter than table sugar, which makes it about as sweet as aspartame (32).  It is often blended with other artificial sweeteners (33).

History

Acesulfame Potassium was discovered accidentally (like most of the sugar substitutes) by Karl Clauss and Harald Jensen in 1967 in Germany.  It was named acesulfame potassium by the WHO in 1978, and it was on American tabletops as a sweetener by 1988 (32).

Mode of Action

Acesulfame potassium (Potassium 6-methyl-2,2-dioxo-2H-1,2λ6,3-oxathiazin-4-olate) is a sulfamate ester and a potassium salt (34).

After ingestion, acesulfame potassium passes through the body quickly without being metabolized.  It is excreted unchanged through the kidneys (34).

Common Products

Acesulfame potassium can be found in baked goods, frozen desserts, dry cereal, chewing gum, condiments, beverages, candy, and dog toothpaste.  It is present in a number of baked goods requiring a sugar substitute, due to its heat stable properties.  It is also approved for use as a flavor enhancer in food but not in poultry or meat (16).

Safety and Side Effects

  • Potential Cancer Risk

Acesulfame potassium has been implicated, as all artificial sweeteners have, in being carcinogenic, but long-term exposure in animal studies did not cause cancer in laboratory animals.  To date, the risk of cancer in humans has not been assessed yet, leading to some distrust of its safety profile (34).

  • Acesulfame Potassium could raise insulin levels—no long term evidence is clear yet

In a 1987 animal study, extremely high doses of acesulfame potassium delivered intravenously to rats resulted in a large release of insulin (35).  However, when studied in humans, it was not found to cause an increase in insulin– but the study was not long-term.  Many people feel that the studies were not sufficient to determine how it could impact humans in the long term (36).

  • Acesulfame potassium passes through breast milk

In a study of lactating women who consumed artificial sweeteners, acesulfame potassium was named as one of the nonnutritive sweeteners found in breast milk (37).

Again, if you are the slightest bit concerned about consuming acesulfame potassium, there are many other choices that can take the place of sugar.

Sucralose

Sucralose is one of the most popular artificial sweeteners on the market today.  It is known as Splenda, Sukrana, Zerocal, Candys, SucraPlus, Nevella, and Cukren.  It is 320-1,000 times sweeter than sugar, making it 3x sweeter than aspartame or acesulfame potassium (38).

History

Sucralose was found through the research of sucrose and its derivatives.  In 1976, sucrose was added to a chlorine molecule, and it increased the sweetness of sugar dramatically.  It was approved for use in Canada, Australia, and New Zealand in the early 1990s and in the U.S. by 1998.  It was slower to be approved in the European Union which did not approve it until 2004.  In 2006, the US FDA ruled that it had to adhere to the regulations for foods containing sucralose and must be classified as a nonnutritive sweetener (38).

Mode of Action

Sucralose (2R,3R,4R,5R,6R)-2-[(2R,3S,4S,5S)-2,5-bis(chloromethyl)-3,4-dihydroxyoxolan-2-yl]oxy-5-chloro-6-(hydroxymethyl)oxane-3,4-diol) is a disaccharide derivative containing two units linked by a glycosidic bond.  4-chloro-4-deoxy-alpha-D-galactopyranose and 1,6-dichloro-1,6-dideoxy-beta-D-fructofuranose are linked together as a chlorinated form of table sugar (sucrose) (39).

It is processed through selective chlorination which replaces sucrose’s naturally existing hydroxyl groups with chlorine atoms.  During the chlorination process the sugar is partially acetylated.  Then the acetyl groups are removed, resulting in the end product of sucralose (38).

In powdered form, sucralose is often bulked up to 95% of its volume with either maltodextrin or dextrose, as it is in the brand-name product Splenda. The addition of these fillers is one reason why sucralose affects insulin levels (38).

After ingestion, most of the sucralose passes through the digestive system intact and unchanged, with only a very small portion being absorbed from the body.  The portion that is absorbed is quickly eliminated.  Sucralose does not break down within the body or separate from the chlorine (40).

Common Products

Sucralose is found as a tabletop sweetener, in breakfast bars, canned fruits, beverages, baked goods, soft drinks, chewing gum, condiments, and syrups (38).

It is heat stable and retains its’ sweetness, so it is a popular substitute for sugar when baking.  In order to make sucralose in granulated form to be used in same-volume substitution for sugar, it has to be bulked with fillers.  These fillers dissolve in water rapidly and can cause baked products to have the same sweetness of sugar, but they lose moisture and texture (38).

Unlike sugar, sucralose maintains its granular structure in dry temperatures like in ovens.  Sugar will melt when baked; but because sucralose does not, it will not melt or crystallize because it starts to decompose around 246 degrees Fahrenheit. This can make certain textures and techniques unachievable with sucralose as a sugar substitution in some cooking and baking (38).

Despite its advantages in baking, there are some safety concerns with sucralose when included in baking products, and it’s recommended to use a different artificial sweetener when baking above 350°F (175°C) (See our Safety and Side Effects section below for more information)(41)(42)(43).

Safety and Side Effects

  • Sucralose can raise blood sugar levels

Based on mixed results from different studies, the effect that sucralose will have on your blood sugar will vary depending on how much you’re used to consuming.

A study in obese participants who did not regularly consume sucralose found that their blood sugar levels became elevated by 14%, and their insulin levels were elevated by 20% after ingestion (44).

However, studies of people who regularly consumed sucralose proved incongruous and found little to no effect on blood sugar (45)(46).

  • Sucralose raises insulin levels

A study in healthy adults found that after they were given sucralose, the results on a glucose tolerance test showed a 20% higher blood insulin level which was slower to be eliminated from their bodies.  It is currently believed that because the sweet taste receptors are triggered by sucralose that an effect called “cephalic phase insulin release” occurs which triggers a release of insulin (47).

When sucralose bypasses the mouth and is delivered straight into the stomach, the insulin levels do not change (45).

  • Sucralose reduces the good bacteria in the gut

Sucralose, in the Splenda form, decreases the beneficial bacteria in the gut after 12-week administration in rats (44).

No human studies are available to correlate these findings in people.

  • Sucralose may be harmful when used in baking

Splenda begins to break down and interact with other ingredients and compounds present at high temperatures (41).

When Splenda is baked in food, harmful substances can be produced.  Mixing sucralose and a compound from fat called glycerol (as fat is commonly used in baked goods) resulted in the formation of chloropropanols.  Chloropropanols have been implicated in increasing cancer risk (48).

  • Sucralose passes through breastmilk

Sucralose has been detected in breastmilk (37).

Again, if using sucralose concerns you, we will go over some other alternatives which may be a better choice for you.

Stevia

Stevia is a sugar alternative that is derived from a plant.  The stevia plant has been used in other countries like Japan for many decades before it gained popularity elsewhere in the world.  Stevia leaf itself is rarely used, but instead extracts of stevia are what you’re most likely consuming when you use a product labeled stevia.  The stevia plant (Stevia rebaudiana) is native to South America and is grown in Paraguay, China, Japan, Brazil, and the United States (49)(50).

Its botanical names include Yerba Dulce, Sweet Herb of Paraguay, Estevia, Green Stevia, Azucacaa, and Kaa Jhee (51).

You may know it by the brands Truvia, PureVia, SweetLeaf, SplendaNaturals Stevia, and Stevia In the Raw.  Stevia is 250-300 times sweeter than table sugar (52).

It is the only nonnutritive sweetener that is also labeled as a dietary supplement, though this was mostly due to regulatory labeling criteria.

History

Stevia has been used by the indigenous populations of South America for over 1,500 years.  The Guaraní tribe called stevia the “sweet herb.”  In Brazil and Paraguay, the leaves of the stevia plant have been used as both medicine and as a sweetener for teas.

Stevia earned its name from a sixteenth-century Spanish physician, Pedro Jaime Esteve, who was a botanist and professor at the University of Valencia.

Though stevia’s sweet taste was known traditionally, it only began to have true chemical analysis after the turn of the twentieth century.  In 1931, the chemical constituents of stevia which give it its sweet taste, glycosides, were isolated by French chemists (50).

Stevia has been hailed as an all-natural sweetener that has a very low toxicity; but even so, it was banned as recently as the 1990s by the U.S. FDA.  Studies indicated that steviol, a glycoside, can be converted into a compound which promotes mutagenicity.  The European Union also did not endorse stevia in the late 1990s.  Though this has now changed, in 1995 the FDA ruled that stevia could be used only as a dietary supplement (53).

Much of the discrepancies in stevia’s legal status are derived from the differences between consuming stevia leaves versus their safer extracts.  Stevia leaves (called crude stevia) and crude stevia extracts are not approved for use in food.  Only high-purity steviol glycosides are approved for use in food and have been recognized as GRAS substances “Generally Recognized as Safe” since 2008 (54)(50).

Despite the ability to grow your own stevia plant at home, it is extremely discouraged that you use this form of whole leaf stevia for any form of dietary consumption.

Mode of Action

The sweet components of the stevia leaf come from its glycosides, often called steviol glycosides. Stevia leaves contain over 40 compounds which contribute to its sweetness, but the glycosides are primarily responsible for its taste.  The stevia that is available for use in foods and beverages is a purified leaf extract which can contain one or more of these glycoside extracts (52).

Glycosides are molecules that retain glucose residues bound to other molecules called aglycones.  The taste receptors on the tongue react to the glycosides by direct activation of the sweet receptors.  Unfortunately, stevia can often have a bitter aftertaste because glycosides also activate the bitter receptors of the tongue (50).

After ingestion, steviol glycosides are not absorbed.  The steviol passes through the digestive tract and into the bloodstream, carried to the liver where it is metabolized into steviol glucuronide, and it is eliminated in urine (50).

The ten main steviol glycosides are:  Stevioside, Steviolbioside, [Rebaudioside A, B, C, D, E, F], Rubusoside, and Dulcoside A.  They are extracted from the leaves via water or alcohol extraction where the dried plant leaves are steeped in water.  The water is then filtered and purified with the addition of water or alcohol.  The end-product is a white substance that contains 95% steviol glycoside (55).

Some of the glycosides have different taste properties, such as Rebaudioside D which has the cleanest taste and most closely resembles the taste of sugar.  Other glycosides can have a metallic, bitter, or licorice-like taste, like the glycoside stevioside.  As there are many different flavors of glycosides, using a whole leaf extract which contains all of the glycosides is not used as a pure substitute for sugar because of the competing tastes (52).

Since stevia extracts are so potent, they are often mixed with other artificial sweeteners.  A sugar alcohol, such as erythritol, or carbohydrates like maltodextrin or dextrose, are often added to help mellow out the sharpness of stevia’s sweet taste (52).

Common Products

Most stevia on the shelf today contains Rebaudioside A (often abbreviated on labels and ingredients lists as Reb-A or Rebiana) (50).  This was the most common type of stevia extract available from 2008.  In 2016, Splenda developed a product line called Splenda Naturals which contained Rebaudioside D.  One of the most popular brands, SweetLeaf, contains both Reb-A and Reb-D (52).  Truvia contains rebiana combined with erythritol, and PureVia is rebiana branded by the PepsiCo company (50).

Steviol extracts are heat stable, making them popular for use in baked goods (50).  Stevia is used as a tabletop sweetener, in beverages, baked goods, pre-packaged granola bars, breakfast cereals, and many more products.

Safety and Side Effects

The biggest thing to remember with stevia is that it is approved and recognized as a safe substance, but it depends on which form.  Crude or whole-leaf stevia and crude stevia extracts are not recognized as safe for foods or beverages.  This is due to a lack of information on crude stevia and the concern that crude, or raw, stevia could damage the kidneys and cardiovascular and reproductive systems.

  • Potential Cancer Risk

The glycoside steviol in high doses may weakly increase mutagenic activity, per the Memorial Sloan Kettering Cancer Center, but there are no carcinogenicity publications for Rebaudioside A (Reb-A) or stevioside.  However, the acceptable daily intake of steviol glycosides is up to 4 mg/kg of body weight that is deemed safe by the World Health Organization’s Joint Experts Committee on Food Additives (50).

  • DO NOT USE IF ALLERGIC TO RAGWEED

Stevia belongs to the Asteraceae/Compositae family of plants which includes ragweed, daisies, marigolds, and chrysanthemums, and it is not recommended to consume stevia if you have an allergy to any plants in this family (61).

  • Stevia may disrupt your gut flora

Stevia in the Reb-A form disrupted the microbiota gut flora by reducing the amount of beneficial bacteria present in the microbiome (62).

  • Certain forms of Stevia mixed with sugar alcohols can cause digestive upset

Not all forms of stevia are mixed with sugar alcohols, like erythritol, but the extracts that are combined with sugar alcohols can sometimes cause bloating, diarrhea, and digestive complaints in people who may be sensitive to sugar alcohols.

  • Whole-leaf, crude, or raw stevia should not be used while pregnant

Only Reb-A has been thoroughly studied and approved for use in pregnant women.

Monk Fruit

Monk Fruit or Luo Han Guo (Siraitia grosvenorii, Momordica grosvenori) is a fruit which grows on a vine that has been used traditionally in China and Thailand since the 13th century.  A member of the gourd (Cucurbitaceae) family, an extract of its fruit is about 300 times sweeter than table sugar (63).

While you may not have heard of it, it has been the sweetening agent in many Asian soft drinks for a long time.  You can now find it making its way into more products across the world, and you can purchase the extract in a granular form perfect for tabletop use or in baking.

Common names are Monk Fruit in the Raw, Nectresse, Fruit-Sweetness, Purefruit, PureLo, and Lakanto.

History

Monk Fruit earned its name because of the Chinese monks in Guangxi who first mentioned the plant in their writings in the 13th century.  It also goes by the name of “Buddha fruit” or “longevity fruit” because of its loose translation from Sanskrit into Chinese.  It is closely linked in the Buddhist traditions of the monks in China (63).

The fruit began to earn notable mentions in the western world in 1938 when it was discussed in a manuscript by G. Weidman Groff.  Groff described the use of it for maladies related to overheating.  Monk Fruit was described as a cooling substance that was being used to treat inflammation, fever, or to provide relief from hot temperatures (63).

Monk Fruit was introduced to the United States in the early part of the 20th century.  By 1917, the ministry of agriculture was already showing interest in the plant, and it was making its way through botany societies.  Frederick Coville, a botanist, showed the plant to Groff which he had purchased in Washington, D.C.  In 1941, the species was entered into botanical descriptions of the time.

The sweetness of Monk Fruit began to garner interest around 1975 when it was discovered by C. H. Lee.  The plant was studied by the Japanese in the 1980s by Tsunematsu Takemoto and further developed (63).

Mode of Action

Monk Fruit’s sweetness is due to its glycosides, called mogrosides.  Like other plant glycosides, mogrosides contain glucose residues attached to another molecule.  In the case of mogrosides, the glucose residue is attached to a structure called a mogrol (64).

Though what we know about mogrosides is based on animal studies, it is believed that it functions similarly in humans.  The mogrosides in Monk Fruit are not absorbed or metabolized in the upper portion of the digestive system.  Instead, when the mogrosides reach the colon, the gut bacteria go to work.  The gut bacteria separate the mogrol from the glucose residue/molecule and use the glucose for energy.  The mogrol is then excreted mostly from the body via the gastrointestinal tract with a very small amount absorbed in the bloodstream and then excreted in the urine (64).

Monk Fruit is stable at high temperatures, so it is often used in baking (64).

Common Products

Monk Fruit is found in beverages, candies, dairy products, baked goods, and as a tabletop sweetener (64).  In countries where it is native, like Thailand and China, you may find it its whole fruit form, but it is unlikely to find the whole fruit elsewhere.

Safety and Side Effects

There have been no negative side effects observed with extremely large doses of monk fruit in animals (80). It is considered a GRAS (Generally Recognized as Safe) substance by the U.S. FDA. since 2010 (64).

Conclusion

Humans have consumed forms of natural sugars for millennia.  Much like our recent discoveries of sugar substitutes have almost always been accidental, early humans were likely surprised from that first taste of fruit.  Since then, sweetness has been a part of the human palette.  Cultivation of sweetness from gathering wild fruits, keeping bees for honey, and munching on wild sugarcane has been part of our relationship with food since the beginning.

As our desire for sweetness really began to go from occasional to ordinary, due to trading in the fifteenth and sixteenth centuries, we have seen more and more health problems occurring.  From the fashionable practice of blackened teeth in the Elizabethan era and its belief that even sugar itself could be used as a toothpaste, we can see how being overly zealous about sugar becoming accessible has set us up for problems, the likes of which our ancestors were simply not aware.

Now we understand that sugar can lead to a host of ailments, and we educate one another about balanced dietary practices.  However, you generally can’t get something for nothing—and we are also becoming aware of how synthetic choices for sugar can also lead to inadvertent and undesirable consequences.

There are more natural sugar alternatives available, such as stevia and monk fruit, which are less synthetic and have not proved to be as problematic as some of the chemically engineered sugar substitutes.

Just like with regular sugar, the poison is in the dose:  sugar substitutes should not be used in excess or blithely consumed as free substances.  Like everything in a balanced diet, moderation should be key.  When you need that sweet taste, think critically about the amounts and read labels, and consider your options as a consumer.

References

  1. Skerett, Patrick J. “Is Fructose Bad for You?” https://www.health.harvard.edu/blog/is-fructose-bad-for-you-201104262425.
  2. “Background on Carbohydrates & Sugars.” International Food Information Council Foundation, https://foodinsight.org/background-on-carbohydrates-sugars/.
  3. Hess-Fischl, Amy. “What Is Insulin?” https://www.endocrineweb.com/conditions/type-1-diabetes/what-insulin.
  4. Thomas, Liji. “What’s the Difference Between Fructose and Glucose?” https://www.news-medical.net/health/Whats-the-Difference-Between-Fructose-and-Glucose.aspx.
  5. Ancira, Kimberly. “What Is the Difference Between Sucrose, Glucose & Fructose?” https://healthyeating.sfgate.com/difference-between-sucrose-glucose-fructose-8704.html.
  6. Steen, Juliette. “Difference Between Fructose, Glucose And Sucrose.” https://www.huffingtonpost.com.au/2016/06/28/sugars-the-difference-between-fructose-glucose-and-sucrose_a_21420843/.
  7. “Polysaccharide.” Wikipedia, https://en.wikipedia.org/wiki/Polysaccharide.
  8. “Oligosaccharide.” Wikipedia, https://en.wikipedia.org/wiki/Oligosaccharide.
  9. “What Is the Difference between Glucose, Fructose and Sucrose?” World of Molecules, https://www.worldofmolecules.com/3D/what-is-the-difference-between-sucrose-and-fructose.html.
  10. Fung, Jason. “Fructose and Fatty Liver – Why Sugar Is a Toxin.” https://www.dietdoctor.com/fructose-fatty-liver-sugar-toxin.
  11. Patel, Kamal. “What Is the Difference between High Fructose Corn Syrup (HFCS) and Sugar?” 13 Jan. 2020, https://examine.com/nutrition/difference-between-hfcs-and-sugar/.
  12. “Galactose.” https://www.sciencedirect.com/topics/neuroscience/galactose.
  13. “Malt.” Wikipedia, https://en.wikipedia.org/wiki/Malt.
  14. Nill, Ashley. “The History of Aspartame (2000 Third Year Paper).” https://dash.harvard.edu/bitstream/handle/1/8846759/Nill,_Ashley_-_The_History_of_Aspartame.pdf?sequence=3.
  15. “Encyclopedia of Food Sciences and Nutrition 2nd Edition.” https://www.elsevier.com/books/T/A/9780122270550.
  16. “Additional Information about High-Intensity Sweeteners Permitted for Use in Food in the United States.” FDA, https://www.fda.gov/food/food-additives-petitions/additional-information-about-high-intensity-sweeteners-permitted-use-food-united-states.
  17. “Saccharin.” Wikipedia, https://en.wikipedia.org/wiki/Saccharin.
  18. “Saccharin.” NIH PubChem, https://pubchem.ncbi.nlm.nih.gov/compound/SACCHARIN.
  19. Okoduwa, S.I.R., et al. “The Metabolism and Toxicology of Saccharin.” July 2013, https://www.researchgate.net/publication/304354526_The_Metabolism_and_Toxicology_of_Saccharin.
  20. Suez, J, et al. “Artificial Sweeteners Induce Glucose Intolerance by Altering the Gut Microbiota.” Nature, vol. 514, no. 7521, 9 Oct. 2014, doi:10.1038/nature13793.
  21. Suez, J, et al. “Non-Caloric Artificial Sweeteners and the Microbiome: Findings and Challenges.” Gut Microbes, vol. 6, no. 2, 2015, pp. 149–155., doi:10.1080/19490976.2015.1017700.
  22. Sylvetsky, Allison C et al. “Nonnutritive Sweeteners in Breast Milk.” Journal of toxicology and environmental health. Part Avol. 78,16 (2015): 1029-32. doi:10.1080/15287394.2015.1053646
  23. “Sweeteners.” Virtual Chembook, http://chemistry.elmhurst.edu/vchembook/549sweet.html.
  24. “Aspartame.” NIH PubChem, https://pubchem.ncbi.nlm.nih.gov/compound/Aspartame.
  25. Edwards, Rebekah. “Aspartame: 11 Dangers of This All-Too-Common Food Additive.” 13 May 2019, https://draxe.com/nutrition/aspartame/.
  26. Soffritti, Morando, et al. “First Experimental Demonstration of the Multipotential Carcinogenic Effects of Aspartame Administered in the Feed to Sprague-Dawley Rats.” Research, 1 Mar. 2006, doi:https://doi.org/10.1289/ehp.8711.
  27. “Artificial Sweeteners and Cancer.” National Cancer Institute, https://www.cancer.gov/about-cancer/causes-prevention/risk/diet/artificial-sweeteners-fact-sheet.
  28. “Bad Science From Harvard.” American Council on Science and Health, 25 Oct. 2012, https://www.acsh.org/news/2012/10/25/bad-science-from-harvard.
  29. “Phenylketonuria.” Wikipedia, https://en.wikipedia.org/wiki/Phenylketonuria.
  30. Schultz, Jacob, et al. “Consumption of Aspartame Associated with Tardive Dyskinesia New Observation.” Journal of Clinical Psychopharmacology, vol. 39, no. 6, 12 Nov. 2019, pp. 690–691., doi:doi: 10.1097/JCP.0000000000001112.
  31. Lohner, Szimonetta et al. “Health outcomes of non-nutritive sweeteners: analysis of the research landscape.” Nutrition journal vol. 16,1 55. 8 Sep. 2017, doi:10.1186/s12937-017-0278-x
  32. “Acesulfame Potassium.” Wikipedia, https://en.wikipedia.org/wiki/Acesulfame_potassium.
  33. “Acesulfame Potassium.” NIH PubChem, https://pubchem.ncbi.nlm.nih.gov/compound/Acesulfame potassium.
  34. “Acesulfame.” NIH PubChem, https://pubchem.ncbi.nlm.nih.gov/compound/acesulfame.
  35. Liang, Y, et al. “The Effect of Artificial Sweetener on Insulin Secretion. 1. The Effect of Acesulfame K on Insulin Secretion in the Rat (Studies in Vivo).” Horm Metab Res., vol. 19, no. 6, June 1987, pp. 233–8., https://www.ncbi.nlm.nih.gov/pubmed/2887500.
  36. Pepino, Marta Y, and Christina Bourne. “Non-nutritive sweeteners, energy balance, and glucose homeostasis.” Current opinion in clinical nutrition and metabolic care vol. 14,4 (2011): 391-5. doi:10.1097/MCO.0b013e3283468e7e
  37. Sylvetsky, Allison C et al. “Nonnutritive Sweeteners in Breast Milk.” Journal of toxicology and environmental health. Part A vol. 78,16 (2015): 1029-32. doi:10.1080/15287394.2015.1053646
  38. “Sucralose.” Wikipedia, https://en.wikipedia.org/wiki/Sucralose.
  39. “Sucralose.” NIH PubChem, https://pubchem.ncbi.nlm.nih.gov/compound/71485.
  40. “FAQs.” Sucralose.org, https://sucralose.org/faqs/.
  41. Schiffman, Susan S, and Kristina I Rother. “Sucralose, a synthetic organochlorine sweetener: overview of biological issues.” Journal of toxicology and environmental health. Part B, Critical reviews vol. 16,7 (2013): 399-451. doi:10.1080/10937404.2013.842523
  42. Bannach, Gilbert, et al. “Thermal Stability and Thermal Decomposition of Sucralose.” Ecletica Quimica, vol. 34, no. 4, Dec. 2009, doi:http://dx.doi.org/10.1590/S0100-46702009000400002 .
  43. 43. de Oliveira, Diogo N et al. “Thermal degradation of sucralose: a combination of analytical methods to determine stability and chlorinated byproducts.” Scientific reports vol. 5 9598. 15 Apr. 2015, doi:10.1038/srep09598
  44. Abou-Donia, Mohamed B., et al. “Splenda Alters Gut Microflora and Increases Intestinal P-Glycoprotein and Cytochrome P-450 in Male Rats.” Journal of Toxicology and Environmental Health, Part A, vol. 71, no. 21, 2008, doi:https://doi.org/10.1080/15287390802328630.
  45. 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, vol. 296, no. 4, Apr. 2009, 10.1152/ajpgi.90708.2008.
  46. 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., vol. 65, no. 4, Apr. 2011, doi:10.1038/ejcn.2010.291.
  47. Pepino, MY, et al. “Sucralose Affects Glycemic and Hormonal Responses to an Oral Glucose Load.” Diabetes Care, vol. 36, no. 9, Sept. 2013, doi:10.2337/dc12-2221.
  48. Rahn, Anja, and Varoujan A. Yaylayan. “Thermal Degradation of Sucralose and Its Potential in Generating Chloropropanols in the Presence of Glycerol.” Food Chemistry, vol. 118, no. 1, 1 Jan. 2010, pp. 56–61., doi:https://doi.org/10.1016/j.foodchem.2009.04.133.
  49. “Stevia Farming.” PureCircle Stevia Institute, https://www.purecirclesteviainstitute.com/agriculture/stevia-farming.
  50. “Stevia.” Wikipedia, https://en.wikipedia.org/wiki/Stevia.
  51. “Stevia.” MedlinePlus, https://medlineplus.gov/druginfo/natural/682.html.
  52. “How Sweet is Stevia.” PureCircle Stevia Institute, https://www.purecirclesteviainstitute.com/healthy-lifestyle/great-taste/how-sweet-is-stevia.
  53. Tandel, Kirtida R. “Sugar substitutes: Health controversy over perceived benefits.” Journal of pharmacology & pharmacotherapeutics vol. 2,4 (2011): 236-43. doi:10.4103/0976-500X.85936
  54. “Has Stevia Been Approved by FDA to Be Used as a Sweetener?” FDA, https://www.fda.gov/about-fda/fda-basics/has-stevia-been-approved-fda-be-used-sweetener.
  55. “Steviol Glycosides.” International Stevia Council, http://www.internationalsteviacouncil.org/index.php?id=196.
  56. Paul, S, et al. “Stevioside Induced ROS-Mediated Apoptosis through Mitochondrial Pathway in Human Breast Cancer Cell Line MCF-7.” Nutr Cancer, vol. 64, no. 7, 2012, pp. 1084–94., https://www.ncbi.nlm.nih.gov/pubmed/23061910.
  57. Ukiya, Motohiko, et al. “Cytotoxic and Apoptosis‐Inducing Activities of Steviol and Isosteviol Derivatives against Human Cancer Cell Lines.” Chemistry & Biodiversity, vol. 10, no. 2, 18 Feb. 2013, https://onlinelibrary.wiley.com/doi/abs/10.1002/cbdv.201200406.
  58. Hsieh, Ming-Hsiung, et al. “Efficacy and Tolerability of Oral Stevioside in Patients with Mild Essential Hypertension: A Two-Year, Randomized, Placebo-Controlled Study.” Clinical Therapeutics, vol. 25, no. 11, Nov. 2003, pp. 2797–2808., doi:https://doi.org/10.1016/S0149-2918(03)80334-X.
  59. Anton, Stephen D et al. “Effects of stevia, aspartame, and sucrose on food intake, satiety, and postprandial glucose and insulin levels.” Appetite vol. 55,1 (2010): 37-43. doi:10.1016/j.appet.2010.03.009
  60. Sharma, N., et al. “Effect of Stevia Extract Intervention on Lipid Profile.” Ethno-Med, vol. 3, no. 2, 2009, pp. 137–140., http://www.krepublishers.com/02-Journals/S-EM/EM-03-0-000-09-Web/EM-03-2-000-2009-Abst-PDF/EM-03-2-137-09-047-Sharma-N/EM-03-2-137-09-047-Sharma-N-Tt.pdf.
  61. “Stevia.” https://www.rxlist.com/stevia/supplements.htm.
  62. Nettleton, Jodi E et al. “Low-Dose Stevia (Rebaudioside A) Consumption Perturbs Gut Microbiota and the Mesolimbic Dopamine Reward System.” Nutrients vol. 11,6 1248. 31 May. 2019, doi:10.3390/nu11061248
  63. “Siraitia Grosvenorii.” Wikipedia, https://en.wikipedia.org/wiki/Siraitia_grosvenorii.
  64. “Everything You Need to Know about Monk Fruit Sweeteners.” International Food Information Council Foundation, https://foodinsight.org/everything-you-need-to-know-about-monk-fruit-sweeteners/.
  65. Li, C, et al. “Chemistry and Pharmacology of Siraitia Grosvenorii: a Review.” Chin J Nat Med., vol. 12, no. 2, Feb. 2014, pp. 89–102., https://www.ncbi.nlm.nih.gov/pubmed/24636058.
  66. Chiang, John Y L. “Bile acid metabolism and signaling.” Comprehensive Physiology vol. 3,3 (2013): 1191-212. doi:10.1002/cphy.c120023
  67. “Mogroside Cholesterol.” https://www.ncbi.nlm.nih.gov/pubmed/?term=mogroside cholesterol.
  68. Lin, GP, et al. “Effect of Siraitia Grosvenorii Polysaccharide on Glucose and Lipid of Diabetic Rabbits Induced by Feeding High Fat/High Sucrose Chow.” Exp Diabetes Res., vol. 67435, 2007, doi:10.1155/2007/67435.
  69. Suzuki, YA, et al. “Triterpene Glycosides of Siraitia Grosvenori Inhibit Rat Intestinal Maltase and Suppress the Rise in Blood Glucose Level after a Single Oral Administration of Maltose in Rats.” J Agric Food Chem., vol. 53, no. 8, 20 Apr. 2005, pp. 2941–6., https://www.ncbi.nlm.nih.gov/pubmed/15826043.
  70. Suzuki, YA, et al. “Antidiabetic Effect of Long-Term Supplementation with Siraitia Grosvenori on the Spontaneously Diabetic Goto-Kakizaki Rat.” Br J Nutri., vol. 97, no. 4, Apr. 2007, pp. 770–5., https://www.ncbi.nlm.nih.gov/pubmed/17349091.
  71. Hossen, MA, et al. “Effect of Lo Han Kuo (Siraitia Grosvenori Swingle) on Nasal Rubbing and Scratching Behavior in ICR Mice.” Biol Pharm Bull., vol. 28, no. 2, Feb. 2005, pp. 238–41., https://www.ncbi.nlm.nih.gov/pubmed/15684476.
  72. Zheng, Y, et al. “A New Antibacterial Compound from Luo Han Kuo Fruit Extract (Siraitia Grosvenori).” J Asian Nat Prod Res., vol. 11, no. 8, Aug. 2009, pp. 761–5., https://www.ncbi.nlm.nih.gov/pubmed/20183321.
  73. Zheng, Y, et al. “Antibacterial Compounds from Siraitia Grosvenorii Leaves.” Nat Prod Res., vol. 25, no. 9, May 2011, pp. 890–7., https://www.ncbi.nlm.nih.gov/pubmed/21547839.
  74. Liu, C, et al. “Antiproliferative Activity of Triterpene Glycoside Nutrient from Monk Fruit in Colorectal Cancer and Throat Cancer.” Nutrients, vol. 8, no. 6, 13 June 2016, https://www.ncbi.nlm.nih.gov/pubmed/27304964.
  75. Liu, C et al. “A natural food sweetener with anti-pancreatic cancer properties.” Oncogenesisvol. 5,4 e217. 11 Apr. 2016, doi:10.1038/oncsis.2016.28
  76. Takasaki, M, et al. “Anticarcinogenic Activity of Natural Sweeteners, Cucurbitane Glycosides, from Momordica Grosvenori.” Cancer Lett., vol. 198, no. 1, 30 July 2003, pp. 37–42., https://www.ncbi.nlm.nih.gov/pubmed/12893428.
  77. Rong, Di, and Mou-Tuan Huang. “Anti-Inflammatory Activities of Mogrosides from Momordica Grosvenori in Murine Macrophages and a Murine Ear Edema Model.” Journal of Agricultural and Food Chemistry, vol. 59, no. 13, 1 June 2011, pp. 7474–7481., https://pubs.acs.org/doi/abs/10.1021/jf201207m.
  78. Wang, Q, and K Wang. “[Regulation on the Immunological Effect of Mogrosides in Mice].” Zhong Yao Cai, vol. 24, no. 11, Nov. 2001, pp. 811–2., https://www.ncbi.nlm.nih.gov/pubmed/15575165.
  79. Liu, Da-Duo et al. “Effects of Siraitia grosvenorii Fruits Extracts on Physical Fatigue in Mice.” Iranian journal of pharmaceutical research : IJPRvol. 12,1 (2013): 115-21.
  80. Qin, X, and S. Xiaojian. “Subchronic 90-Day Oral (Gavage) Toxicity Study of a Luo Han Guo Mogroside Extract in Dogs.” Food and Chemical Toxicology, vol. 44, no. 12, Dec. 2006, pp. 2106–2109., https://www.sciencedirect.com/science/article/pii/S027869150600216X?via=ihub.

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