How Sweet It Is: Sweeteners in Breast Milk

Acesulfame

Acesulfame is about 200 times as sweet as sucrose. It is completely absorbed after oral ingestion and is excreted unchanged in the urine over 24 hours. No well-controlled studies are available on the extent of passage of acesulfame into breast milk. However, acesulfame has been found in variable concentrations in the breast milk of nursing mothers.

In a questionnaire study, 20 lactating women completed background questionnaires about breastfeeding and the intake of nonnutritive sweeteners in the previous 24 hours. Each then donated a milk sample that was analyzed for the presence of nonnutritive sweeteners. Sweetener intake was primarily from diet sodas and sweetener packets. Of the women who reported intake of a nonnutritive sweetener, nine had acesulfame detectable in their breast milk in concentrations ranging from 0.01 to 2.22 mg/L. In addition, four of the six women reporting no nonnutritive sweetener intake also had milk acesulfame levels ranging from 0.02 to 0.09 mg/L, probably from unsuspected sources in processed foods.

In another study, acesulfame was detectable in breast milk in 18% of women after an overnight fast. The women then ingested 12 fluid ounces of a caffeine-free diet cola containing 41 mg acesulfame potassium. Acesulfame first appeared in breast milk 2 hours after ingestion and the peak acesulfame concentration in breast milk usually occurred at about 4 hours after ingestion at a median of 0.945 mg/L. One woman had a very high milk acesulfame concentration of 4.76 mg/L.

Aspartame

Aspartame is 150–200 times as sweet as sucrose. It is rapidly metabolized in the gastrointestinal tract to two amino acids that occur naturally in breast milk, aspartic acid and phenylalanine, so it is not detectable in maternal blood or breast milk after ingestion. A theoretical concern is an increase in phenylalanine in milk for breastfed infants with phenylketonuria.

Six lactating women, an average of 98 days postpartum, were given aspartame or lactose orally in a dose of 50 mg/kg (equivalent to 17 aspartame-sweetened sodas or 100 packets of Equal^® in a 68 kg adult) on 2 separate occasions 2 weeks apart in a randomized, crossover trial. Breast milk phenylalanine levels increased to a maximum of about 6 mg/L between 1 and 8 hours after the dose of aspartame and returned to baseline by about 12 hours after the dose. The authors calculated that if the milk phenylalanine concentration were elevated for 24 hours to the maximum found in this high-dose study, a fully breastfed infant would receive only 0.5 mg/kg daily above the normal intake of 79 mg/kg of phenylalanine that occurs naturally in breast milk. So, amounts that are typically ingested in aspartame-sweetened foods and beverages do not result in any additional risk to breastfed infants with phenylketonuria.

Saccharin

Saccharin is 200–700 times as sweet as sucrose. It is 85–95% absorbed after oral ingestion and excreted unchanged in urine. The unabsorbed portion passes through the gastrointestinal tract and is found in feces.^3,4 In the previously described questionnaire study, of the 14 women who reported intake of a nonnutritive sweetener, 4 had saccharin detectable in their breast milk in concentrations ranging from 0.01 to 1.42 mg/L.

Six lactating women were given 126 mg of saccharin in the form of a 356 mL (12 fluid ounce) soft drink every 6 hours for nine doses. The peak milk saccharin concentration occurred 2 hours after both the first and ninth doses. Milk concentrations varied widely, ranging from <0.2 to 1.1 mg/L after the first dose. Both the peak and average amount in milk increased over time, indicating some accumulation in milk with this regimen. The average elimination half-life from milk was 15 hours on day 1 and 18 hours on day 3, although individual values varied considerably. Using the highest milk concentration in this study, an exclusively breastfed infant would receive a dose of 0.27 mg/kg daily, which is much lower than the 5 mg/kg daily limit suggested as safe by the United States Food and Drug Administration (FDA).

Stevia

Stevia is 200–400 times sweeter than sucrose. It is a mixture of several compounds known as steviol glycosides that are derived from the plant, Stevia rebaudiana. Only highly purified steviol glycosides (e.g., rebaudioside A) are approved by the FDA for use in foods, not whole-leaf or crude stevia products. The steviol glycosides are hydrolyzed to steviol in the colon and steviol is absorbed into the bloodstream. Steviol is then glucuronidated and excreted into the urine. No information exists on the excretion of steviol or its glucuronide into breast milk or on the safety of stevia in nursing mothers or infants.

Sucralose

Sucralose is 400–800 times as sweet as sucrose. It is a synthetic compound made by chemically modifying sucrose. It is only about 15% absorbed from the gastrointestinal tract, and then completely excreted in the urine unchanged.

In the previously mentioned questionnaire study, of the 14 women who reported intake of a nonnutritive sweetener, 3 had sucralose detectable in their breast milk in concentrations ranging from 0.01 to 0.04 mg/L. In another study, sucralose was measured in the breast milk of women after an overnight fast. ⁵ The women then ingested 12 fluid ounces of a caffeine-free diet cola containing 68 mg of sucralose. It was detectable in the milk of 21% of women at baseline and in the milk of all women after the cola. Sucralose first appeared in breast milk 2 hours after ingestion and the median peak concentration milk was 0.08 mg/L at 6 hours after soda ingestion when sampling was discontinued. It appeared that the sucralose concentration in breast milk might still be increasing beyond 6 hours.

Sugar Alcohols

Sugar alcohols, also called polyols, are hydrogenated monosaccharides (e.g., mannitol, sorbitol, and xylitol), disaccharides (e.g., isomalt, lactitol, and maltitol); and mixtures of mono-, di-, and/or oligosaccharides (e.g., hydrogenated starch hydrolysates). ⁶ These compounds are somewhat different from the high-intensity artificial sweeteners in that they have about the same or less sweetness than sucrose, and are thus used in larger quantities. They are used primarily to sweeten sugar-free candies, cookies, and chewing gums. They have a lower glycemic index and insulin response than natural sugars and do not promote tooth decay or demineralization. Because they are incompletely absorbed and partially fermented in the colon, high intake of these compounds can cause intestinal discomfort and diarrhea in the user if taken in large amounts.

No studies that measured any of these sweeteners in breast milk after maternal consumption appear to have been done, although some (e.g., mannitol and sorbitol) have been detected as natural components of milk in small amounts. ⁷

Ultrapotent Sweeteners

Two other highly potent sweeteners are approved in the United States, advantame and neotame, although they are not frequently used. Advantame is about 20,000 times sweeter than sucrose. It is only about 15% absorbed from the gastrointestinal tract and it is absent from plasma 4 hours after ingestion. Neotame is 7,000 to 13,000 times sweeter than sucrose. It is virtually completely absorbed after oral ingestion, but the elimination of neotame is poorly characterized in humans. One of the metabolites of both of these sweeteners is phenylalanine, but with the amounts used in foods, there is no concern in phenylketonuria.^8,9 No information on the excretion of advantame or neotame into breast milk is available.

Fructose

Fructose is a natural sugar, but it does not trigger an insulin response. Instead, it is metabolized in the liver to triglycerides. The high-fructose corn sweetener (HFCS) used in sodas is 60% fructose. Agave syrup is a similar sweetener that is > 80% fructose. Intake of HFCS increases the amount of fructose in breast milk.

A randomized, crossover study of 41 exclusively breastfeeding mothers compared consumption of 592 mL (20 fluid ounces) of Coca-Cola^® containing 65 g of HFCS or a “placebo” of 12 fluid ounces of a diet drink artificially sweetened with acesulfame and containing no calories. ¹⁰ About half of the women had a normal weight and the rest were classified as obese. Baseline milk fructose was about 5 mg/L in both groups. Milk fructose did not increase with the artificially sweetened drink. After the HFCS drink, the peak milk fructose occurred 3 hours after the dose and was almost double the baseline concentration at 9.4 mg/L. It remained elevated above baseline for 5 hours. Normal and obese subjects responded similarly. Breast milk glucose was not increased during the a 6-hour study period in either group, probably because insulin secretion modulated maternal serum glucose levels.

In another study, 25 mothers and their exclusively breastfed infants were studied at 1 and 6 months of age. Milk levels of fructose, glucose, lactose, and insulin were similar at the two time points. A multiple regression analysis found that only milk fructose was associated with excess growth of the infants at 6 months of age. Each 1 mg/L increase in breast milk fructose was associated with a 257 g increase in total body weight, 170 g increase in lean mass, 131 g increase in fat mass, and 5 g increase in bone mineral content. ¹¹

Summary and Implications

Excretion of all sweeteners into breast milk appears to be below conventional toxic thresholds. But, a concern is that increased sweetness of milk might predispose infants to later increased sugar intake and obesity. ¹²

It is probably prudent to limit artificial sweetener consumption while breastfeeding, given the lack of information regarding short- and long-term consequences of exposure during infancy. Aspartame may be the preferable high-intensity artificial sweetener for nursing mothers because it does not appear in milk. Polyols might not be as concerning for sweetening the milk as high-intensity sweeteners. However, a recent randomized trial found that a maternal diet that eliminated sorbitol and markedly reduced fructose as well as other oligo-, di-, and monosaccharides reduced the severity of colic in breastfed infants. The specific roles of polyols and fructose and the mechanism are unclear. ⁷

HFCS, which is found in many nondiet sodas, causes unnatural elevations in milk fructose concentrations. Although the full health implications for infants are not confirmed, maternal HFCS intake may increase the growth rate of breastfed infants, possibly leading to obesity. Although more documentation is needed, maternal HFCS and agave syrup intake should probably be limited during breastfeeding.