Other Names
1,2,3-Propanetriol1,2,3-TrihydroxypropaneE422GlicerolGlycerineGlyceritolGlycérolGlycerolGlycerolumGlycyl alcoholPropane-1,2,3-triolPropanetriolTrihydroxypropaneVegetable glycerinVegetable glycerine
Glycerin, also referred to as glycerol, is a polyhydric sugar alcohol with the chemical name propane-1,2,3-triol, molecular formula C3H8O3, and a molar mass of 92.09 g/mol. The modern use of the word glycerine (alternatively spelled glycerin) refers to commercial preparations of glycerol that are less than 100% pure, typically 95%. Historically called glycerine (or glycerin), that name is considered slightly misleading because the -ine suffix denotes an amine, not an alcohol.
Glycerine is a trihydroxyalcohol, meaning it has three hydroxyl groups (–OH). This chemical structure gives it unique properties such as solubility in water and a strong capacity to retain moisture. It is odourless, colourless, and has a sweet taste. Because of its three hydroxyl groups, glycerol is miscible with water and is hygroscopic in nature. As a sugar substitute, it has approximately 27 kilocalories per teaspoon (compared to sugar's 20) and is approximately 60% as sweet as sucrose.
For human consumption, glycerol is classified by the U.S. FDA among the sugar alcohols as a caloric macronutrient. As a food additive, glycerol is labeled under the E number E422 in the European system.
Glycerin is present in all natural fats, oils, and phospholipids and is the chemical backbone of triglycerides. The most abundant of glycerides are triglycerides (found in animal fats and vegetable oils), the form in which glycerol is most commonly found in nature. While glycerin occurs naturally in plants through the fermentation of sugars, most of the glycerin nowadays is produced from the hydrolysis of fats and oils.
Glycerine can be produced by a number of different methods, but the most common include saponification and transesterification. Saponification involves reacting a fat (such as a vegetable oil) with a strong base (such as caustic soda) to produce soap and glycerine. Transesterification is used primarily in the production of biodiesel, where it transforms the triglycerides in vegetable oils into methyl esters (biodiesel), with glycerine produced as a by-product. A more modern synthetic method involves the chemical synthesis of glycerol from propylene, a petroleum derivative, allowing for production without relying on fats and oils.
The glycerin available in today's market can broadly be categorized into two types: vegetable and synthetic. Vegetable glycerin is derived from plant oils such as soy, palm, or coconut. It is particularly favored in the food, cosmetic, and pharmaceutical industries due to its natural origin, which appeals to consumers seeking plant-based and non-animal-derived products.
Common commercial forms include:
Pioneering Swedish chemist Carl Wilhelm Scheele reported the discovery of glycerol in a 1783 article titled "Findings concerning a particular sweet substance in expressed oils and fatty substances." In doing so, he established that glycerol is sweet-tasting and that it is the alcohol portion of natural mono-, di-, and triglyceride esters. The term glycerin (or glycerine), introduced in 1811 by French chemist Michel-Eugène Chevreul, is ordinarily applied to commercial materials containing more than 95% glycerol. The name glycerine came from the Greek word glykys, meaning "sweet."
In 1823, Chevreul obtained the first patent for a new way to produce fatty acids from fats treated with an alkali, which included the recovery of glycerine released during the process. Théophile-Jules Pelouze (1807–1867) determined glycerol's empirical formula in 1836. Glycerol, originally considered a by-product in the candle and soap production processes, was historically discarded in these manufacturing activities. Until 1948, all glycerol was obtained as a by-product in making soaps from animal and vegetable fats and oils, but industrial syntheses based on propylene or sugar accounted for an increasingly large percentage of production since that time.
Historically, glycerol was first isolated in the 18th century, but its broad utility became more recognized during World War I when it was employed in medical treatments. By the mid-19th century, its therapeutic use in European hospitals was substantial. A 1863 publication in the British medical literature noted that from 1851 to 1861, the annual consumption of glycerine in the Paris hospitals rose from 300 lbs. to 3,000 lbs.
In household surgery, glycerine was known as the best remedy for chapped hands and slight irritation of the face and lips, and was found invaluable in nasal, pudendal, and anal irritation. It was applied in a large number of skin diseases in France, and prominent surgeons used it to dress ulcers and wounds, instead of cerate. It was observed to have apparent antiseptic properties, speedily giving a healthy appearance to foul, unhealthy, and even pultaceous-looking wounds.
Glycerol has also been used in sports drinks to treat dehydration; in skin lotions; in toothpaste and mouthwash; and in drugs that treat a wide range of ailments, including constipation, glaucoma, heart arrhythmia, and angina. It has been administered orally and/or intravenously to reduce intracranial pressure caused by various medical conditions, and has been used to reduce brain volume for neurosurgical procedures.
As long ago as 1945, a book titled Glycerin: Its Industrial and Commercial Applications listed 1,583 specific uses of the compound. In food and beverages, glycerol has served as a humectant, solvent, and sweetener, and may help preserve foods. It is also used as a filler in commercially prepared low-fat foods (e.g., cookies), and as a thickening agent in liqueurs. Glycerol and water are used to preserve certain types of leaves.
Glycerol has three hydroxyl groups responsible for its solubility in water and its hygroscopic nature. The glycerol backbone is central to all lipids known as triglycerides. Glycerol is not merely an exogenous supplement but an endogenous molecule that is a normal product of fat metabolism in the human body.
Glycerol is a key metabolite involved in various physiological processes, including lipid metabolism, gluconeogenesis, and energy homeostasis. Glycerol is the three-carbon backbone molecule for triglycerides (fats/lipids) that are stored in adipose tissue and skeletal muscle. During lipolysis (the breakdown of triglycerides), glycerol is released into circulation along with free fatty acids.
Glycerol metabolism connects lipid metabolism to carbohydrate metabolism by converting glycerol, a product of lipid hydrolysis, into dihydroxyacetone phosphate (DHAP), an intermediate in glycolysis and gluconeogenesis. After triacylglycerol breakdown, glycerol is phosphorylated and oxidized to DHAP, which can enter glycolysis to produce ATP or gluconeogenesis to synthesize glucose for energy storage.
In the liver, glycerol kinase phosphorylates glycerol to form glycerol phosphate. Glycerol phosphate dehydrogenase then oxidizes glycerol phosphate into the glycolytic intermediate DHAP. The liver and kidney, which have high glycerol kinase expression, can directly utilize glycerol for gluconeogenesis, while other tissues like the intestines can convert glycerol to lactate, which then enters the gluconeogenic pathway.
Prolonged fasting or vigorous exercise depletes glycogen stores, making the body switch to de novo glucose synthesis to maintain blood levels. Gluconeogenesis is the process that allows the body to form glucose from non-hexose precursors, particularly glycerol, lactate, pyruvate, propionate, and glucogenic amino acids.
Because of its osmotic properties, which enable greater fluid retention than the ingestion of water alone, glycerol has been proposed as a hyperhydrating agent. Glycerol consumed orally, typically as part of a beverage, creates an osmotic gradient that favors fluid retention. This means that the kidneys, which are responsible for fluid excretion and maintaining fluid and electrolyte balance, will reabsorb more water as the water passes through them.
Glycerol entry into cells is facilitated by aquaglyceroporins such as aquaporin-3 (AQP3), which is expressed in skin and epidermal keratinocytes. Accumulating evidence indicates that the water-, glycerol-, and hydrogen peroxide-transporting channel aquaporin-3 (AQP3) plays a key role in various processes involved in keratinocyte function, and abnormalities in this channel have been observed in several human skin diseases.
Glycerol has a number of effects on skin, acting to increase stratum corneum hydration, improve barrier function and repair, enhance stratum corneum plasticity and distensibility, accelerate desquamation, and inhibit skin irritation. Glycerol entry into epidermal keratinocytes is facilitated by aquaglyceroporins like aquaporin-3 (AQP3), and its conversion to phosphatidylglycerol, a lipid messenger that promotes keratinocyte differentiation, requires the lipid-metabolizing enzyme phospholipase-D2 (PLD2).
Glycerin is known for attracting water to the intercellular space of the skin and protects the lipids of skin cells. Glycerin can also be used as a good solvent for various water-insoluble ingredients and has effective emollient and lubricant properties, including humectant, moisturizing, conditioning, and thickening properties.
As used in foods, glycerol is categorized by the American Dietetic Association as a carbohydrate. The U.S. FDA carbohydrate designation includes all caloric macronutrients excluding protein and fat. Glycerol has a caloric density similar to table sugar, but a lower glycemic index and a different metabolic pathway within the body, so some dietary advocates accept glycerol as a sweetener compatible with low carbohydrate diets. It does not feed the bacteria that form plaques and cause dental cavities.
Small decreases in hydration status can result in a dramatic decrement in athletic performance and greatly increase the risk of thermal injury. Because of its osmotic properties, which enable greater fluid retention than the ingestion of water alone, glycerol has been proposed as a hyperhydrating agent.
Evidence for benefit: In double-blind, randomized, crossover trials performed at an ambient temperature of 23.5–24.5°C, mean heart rate was lower by 2.8 ± 0.4 beats/min (p = 0.05) after glycerol-enhanced hyperhydration in one study and by 4.4 ± 1.1 beats/min (p = 0.01) in a second study. Endurance time was prolonged from 77.4 ± 9 min (control) to 93.8 ± 14 min (glycerol) in the first study (p = 0.049) and from 99.0 ± 11 min to 123.4 ± 17 min in the second study (p = 0.03).
Evidence against or null: It is equivocal whether glycerol hyperhydration improves exercise performance and thermoregulation in the heat. One study compared glycerol with water hyperhydration using a reliable, self-paced variable-intensity cycling protocol under hot, humid conditions, and found no differences in total distance cycled between conditions (29.7 ± 5.7 km for placebo, 28.9 ± 5.7 km for glycerol). Power output was not different at any time between conditions, and terminal rectal temperatures were not significantly different. Similarly, in a tennis-related study, glycerol hyperhydration significantly increased fluid retention by approximately 900 mL over placebo, but although the glycerol hydration regimen provided a better hydration status than placebo, no performance benefits were observed.
The results of glycerol-induced hyperhydration research have been equivocal, most likely because of methodological differences between studies, such as variations in the intensity of exercise, environmental conditions, and concentration or dose of glycerol administered.
Overall assessment: Evidence is mixed. Some well-designed randomized crossover trials support modest improvements in endurance time and cardiovascular efficiency under moderate thermal conditions, while other equally well-designed trials in hot, humid environments show no performance advantage over water alone. A 2025 review of sports supplements noted that glycerol shows positive ergogenic effects supported by strong evidence, especially in endurance sports, while a systematic evidence database notes the inconsistency across conditions. Hydration with glycerol may benefit individuals who are active for prolonged periods in hot environments (e.g., firefighters, military personnel, endurance athletes).
Animal/mechanistic evidence: Orally administered glycerol fully corrected the reduced skin elasticity in aquaporin-3 (AQP3) null mice as measured by the kinetics of skin displacement after suction, and the delayed barrier recovery as measured by transepidermal water loss after tape-stripping. Stratum corneum water content, measured by skin conductance and radioactive water accumulation, was 3-fold lower in AQP3 null vs. wild-type mice, but became similar after topical or systemic administration of glycerol in quantities that normalized stratum corneum glycerol content.
These data provide functional evidence for a physiological role of glycerol transport by an aquaglyceroporin, and indicate that glycerol is a major determinant of stratum corneum water retention, and mechanical and biosynthetic functions.
Human clinical evidence: Endogenous glycerin is believed to be an important component of skin hydration, and topical application of cosmetic products containing glycerin can be associated with improvements in barrier function, induction of biomarkers associated with keratinocyte proliferation and wound healing, reduction in melanin intensity, increases in epidermal thickness, and improvements in general skin appearance. Ichthyosis and xerosis have been relieved by the topical use of glycerin.
Psoriasis (animal model evidence only): Anecdotal reports by patients on the National Psoriasis Foundation website suggest that glycerol may be helpful for the treatment of psoriasis, although no experimental data have confirmed this idea in humans. Research has evaluated whether glycerol inhibits inflammation and psoriasiform lesion development in the imiquimod-induced mouse model of psoriasis, with glycerol provided either in drinking water or applied topically. This represents animal model research only; clinical human trials on glycerol as a psoriasis treatment are lacking.
Wound healing: AQP3-ablated mice showed delayed wound healing of full-thickness skin wounds accompanied by decreased keratinocyte proliferation, and this impairment was rescued through glycerol supplementation. This is preclinical evidence; direct human wound-healing clinical trials with glycerol as the sole intervention are not well established in the peer-reviewed literature.
Overall assessment: Topical glycerin's role as a humectant and skin protectant is well-supported by both mechanistic and observational human evidence. Deeper therapeutic effects (wound healing, psoriasis treatment) are currently based on strong animal/mechanistic data but lack robust human clinical trials.
Glycerin is used as the active ingredient in laxative products (i.e., glycerin suppositories). This product usually produces a bowel movement within 15 minutes to 1 hour. Glycerol's laxative mechanism is primarily osmotic and local: it draws water into the colon and provides mild rectal stimulation. This is an established, widely-accepted pharmaceutical application supported by decades of clinical use and regulatory approval as an OTC drug.
By the oral route, administration of glycerol has been employed to reduce intraocular pressure in cases of glaucoma. One study examined the effect of oral glycerol in 43 eyes suffering from glaucoma of various types. Although glycerol was found to be consistently effective, the effect lasted only temporarily except in cases of primary angle closure. Tension started falling within 10 minutes of glycerol administration in a large number of eyes, and within 30 minutes in most eyes. The lowest limit was reached within one hour, after which tension started increasing again. After 24 hours, tonometric readings were near the pre-glycerol level.
Overall assessment: Glycerol's osmotic properties produce a clinically meaningful but short-lived reduction in intraocular pressure. Its primary ophthalmic application is pre-surgical tension reduction rather than long-term glaucoma management. Evidence base is older and consists primarily of uncontrolled clinical series; modern comparative trials with current IOP-lowering agents are limited.
Glycerin has been administered orally and/or intravenously to reduce intracranial pressure caused by various medical conditions, and has been used to reduce brain volume for neurosurgical procedures. This use is grounded in glycerol's osmotic action — as a hyperosmolar agent, it draws fluid out of brain tissue and into circulation. This is an established pharmaceutical (not supplement) application; dosing and administration are managed in clinical settings.
Glycerol levels, along with those of fatty acids, have been recognized as potential biomarkers for metabolic disorders, particularly hyperglycemia and type 2 diabetes. In type 2 diabetes, increased lipolysis leads to higher circulating glycerol levels, potentially making glycerol an even more significant gluconeogenic substrate contributing to hyperglycemia. Research in this domain is primarily investigational; glycerol is not an established treatment for diabetes.
Glycerol does not feed the bacteria that form plaques and cause dental cavities. It is widely used as a vehicle and humectant in toothpastes and mouthwashes, though its oral-health benefit is primarily functional (vehicle/texture) rather than pharmacologically active in this context.
Dosages below are those reported in specific cited studies or regulatory/clinical references. They should not be construed as recommendations.
Glycerol is generally recognized as safe (GRAS) by the FDA for use in foods. Glycerin is considered generally recognized as safe (GRAS) by the FDA for its use in food packaging and is a multiple-purpose GRAS food substance when used in accordance with good manufacturing practices.
In 1981, the Scientific Committee on Food endorsed the conclusion from the Joint FAO/WHO Expert Committee on Food Additives in 1976 of "acceptable daily intake (ADI) for man not specified." The EFSA Panel concluded that there is no need for a numerical ADI and no safety concern regarding the use of glycerol (E 422) as a food additive at the refined exposure assessment for the reported uses.
Glycerin was not genotoxic in multiple in vitro tests and was not carcinogenic to rats in a long-term feeding study. This ingredient was not a dermal or ocular irritant and was non-sensitizing to guinea pigs or humans. The Cosmetic Ingredient Review Panel noted the high frequency of use reported for glycerin and the low instances of reports of toxicity, irritation, and sensitization in the literature, and the fact that glycerin is GRAS.
No adverse effects were reported in rats receiving doses up to 10,000 mg/kg body weight per day for 1 year, the highest dose tested. There was also no increase in tumour incidences in rats receiving doses up to 5,000 mg/kg body weight per day for 2 years.
The EFSA Panel concluded that glycerol has low acute toxicity and that local irritating effects of glycerol in the gastrointestinal tract reported in some gavage studies were likely due to hygroscopic and osmotic effects of glycerol. Glycerol did not raise concern with respect to genotoxicity and was of no concern with regard to carcinogenicity. Reproductive and prenatal developmental studies were limited to conclude on reproductive toxicity, but no dose-related adverse effects were reported.
At high oral supplemental doses, gastrointestinal adverse effects have been documented. Rectal use may cause rectal discomfort or burning sensation. Oral glycerol at higher doses (as used in sports supplementation) can produce nausea, headache, dizziness, and gastrointestinal discomfort — effects consistent with its osmotic and hygroscopic properties.
Children are at higher risk for side effects from oral glycerol. Glycerol is found in certain flavored drinks, especially slushy ice drinks. Experts recommend that children under 7 years of age should avoid slushies completely. Children who are between 7 and 10 years of age should not drink more than about 1.5 cups (12 ounces) of slushy ice drinks in one day.
The EFSA Panel conservatively estimated the lowest oral dose of glycerol required for therapeutic effect to be 125 mg/kg body weight per hour, and noted that infants and toddlers can be exposed to that dose by drinking less than the volume of one can (330 mL) of a flavoured drink.
Glycerol was included in the WADA list of prohibited substances in 2010 because of its potential use as a masking agent for banned substances in doping tests. However, with the introduction of the biological passport and advancements in detection methods, glycerol was removed from this list in 2017, reinstating its acceptance for use in sports. An athlete who is using fat as their predominant fuel source in an event may actually test positive for glycerol even if they were not supplementing the substance. WADA therefore decided to remove it as a banned substance. As of the current 2025/2026 WADA prohibited list, glycerol is not prohibited.
The source materials and intermediate forms of glycerin (e.g., epichlorohydrin used in synthetic production) should be completely consumed and/or eliminated in the manufacturing process. The FDA has warned that companies should monitor and audit their naturally-derived ingredients because of the potential presence of phorbol esters if the source material is Jatropha.
The FDA has not tested glycerol dietary supplement products to confirm that they contain the ingredients stated on their labels. Purchasers of glycerol-containing dietary supplements should seek products manufactured under verifiable quality standards.
The reasons for glycerol's former prohibition as a masking agent included the potential effect of glycerol in terms of increasing plasma volume and its reported damaging effects on renal functions at high doses. Individuals with existing renal impairment, heart failure, or severe dehydration should exercise caution with high-dose oral glycerol supplementation given its plasma-expanding and osmotic properties. No well-documented herb–drug or supplement–drug pharmacokinetic interactions for glycerol are established in the peer-reviewed literature at normal dietary or cosmetic exposure levels.
Health conditions that Glycerin may help support.
Glycerin (glycerol) is one of the most well-established humectants for dry skin, attracting and retaining water in the stratum corneum. Scientific studies confirm it improves skin moisture content, elasticity, and barrier properties. Research has elucidated its mechanism via aquaporin-3 channels and demonstrated its concentration-dependent moisture-retention capacity.
Glycerin is a humectant emollient central to KP moisturizing formulations, addressing the xerosis and skin barrier dysfunction underlying the condition. Emollients are listed as a first-tier treatment by StatPearls, and glycerin is explicitly cited as a key ingredient in dermatologist-recommended KP emollient products. Adequate skin hydration is a cornerstone of all KP management protocols.
Body systems that Glycerin may help support.