Artificial Sweetener ResearchJune 29, 2011 Written by JP [Font too small?]
At this very moment in laboratories throughout the world there are scientists creating and/or isolating chemicals that the human body will hopefully perceive as sugar. The ultimate goal is to manufacture white crystalline powders that are free of aftertaste, calories and harmful side affects. By achieving this objective, billions upon billions of dollars would be assured. What’s more, consumers, including diabetics, would finally be able to enjoy desserts and sweets of all kinds without fear of health related consequences. Many regulatory agencies in the US and abroad believe such products are already available. They carry names such as NutraSweet, Splenda and Sweet ‘N’ Low. But not all consumer advocacy groups and medical experts agree with this position. Taste issues aside, some of these synthetic sweeteners may not be as safe as they claim.
This year’s American Diabetes Association’s Scientific Sessions featured two studies that may inspire new debate about the safety of aspartame, one of the most popular artificial sweeteners currently on the market. In the first investigation, diet soft drink intake was examined in a group of 474 elderly European and Mexican Americans. The study volunteers had their height, waist circumference and weight examined at the beginning of the research and at three follow-up appointments over a 10 year period. Overall, those who drank diet soft drinks exhibited a 70% greater increase in waist circumference compared to those who didn’t drink diet pop. Participants who drank two or more diet sodas daily averaged increases in waist circumference 500% higher than “non-users”. This is of particular concern because having a larger waist circumference has been repeatedly linked to cardiovascular disease, diabetes and an elevated risk of all-cause mortality.
Here are a few concluding remarks given by the authors of the study: “These results suggest that, amidst the national drive to reduce consumption of sugar-sweetened drinks, policies that would promote the consumption of diet soft drinks may have unintended deleterious effects.” They went on to add: “Data from this and other prospective studies suggest that the promotion of diet sodas and artificial sweeteners as healthy alternatives may be ill-advised”.
The second study presented at the conference was conducted in “diabetes-prone” mice. Two groups of test animals were fed one of two diets: 1) chow enriched with corn oil; 2) chow with added corn oil and aspartame. The mice fed the chow with aspartame were found to have “elevated fasting glucose levels but equal or diminished insulin levels, consistent with early declines in pancreatic beta-cell function”. According to the co-author of the study, Dr. Gabriel Fernandes, “These results suggest that heavy aspartame exposure might potentially directly contribute to increased blood glucose levels, and thus contribute to the associations observed between diet soda consumption and the risk of diabetes in humans”. (1)
While recently perusing the medical literature, I came across other examples of preliminary data about artificial sweeteners (AS) that I find troubling. Here’s a brief review of some the highlights which may help you make up your own mind about this controversial topic:
- Alcoholism Clinical and Experimental Research, May 2011 – Mixing alcohol with diet cola, a very popular combination, hastens intoxication. “Caffeine’s effect on intoxication may be most pronounced when mixers are artificially sweetened, that is, lack sucrose which slows the rate of gastric emptying of alcohol”. (2)
- Molecules and Cells, May 2011 – An in-vitro study examined the effects of three different artificial sweeteners, acesulfame K, aspartame and saccharin on cardioprotective lipoproteins – apolipoprotein A-I and HDL cholesterol. When exposed to the artificial sweeteners, the atheroprotective effects of these lipoproteins changed for the worse. The findings of this first of its kind experiment determined that, “long-term consumption of AS (artificial sweeteners) might accelerate atherosclerosis” and biological aging (senescence) of cells found in connective tissue. (3)
- Food and Chemical Toxicology, June 2011 – Rats fed two dosages of aspartame in their water over a 180 day period exhibited signs of liver stress as indicated by increases in alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and γ-glutamyl transferase (GGT) activity. Antioxidant levels in the liver were also significantly reduced as compared to rats fed only pure water. The conclusion of the trial states, “long term consumption of aspartame leads to hepatocellular injury and alterations in liver antioxidant status mainly through glutathione dependent system”. (4)
The studies listed above are only the tip of the iceberg. In France, researchers from Burgundy University report that some fibromyalgia patients have had “complete regression” of symptoms when aspartame is removed from their diets. In Hungary, an animal study found that a combination of artificial sweeteners results in increased body weight even in the absence of higher food intake. Italian scientists recently revealed that mice that are chronically fed aspartame over their lifetime are more likely to develop liver and lung tumors. Even the most current scientific reviews on both acesulfame potassium (Sunett/Sweet One) and aspartame (Equal/NutraSweet) hesitate to give wholehearted endorsements with regard to safety. (5,6,7,8,9)
Aspartame Affects Insulin Output Differently Than Stevia
Source: Appetite. 2010 August; 55(1): 37–43. (link)
In my opinion, there are just simply too many unanswered questions about artificial sweeteners (AS). Here are three examples that support my sense of uncertainty: 1) The popular AS, sucralose, has a minimal impact on blood sugar. However, it is often sold in products that combine it with a high-glycemic carbohydrate known as maltodextrin. A recent experiment found that this combination does, in fact, increase blood glucose and insulin in healthy human subjects. 2) Feeding mice high saccharin diets stimulates sugary food intake or “bingeing-proness”. 3) Acesulfame-K consumed by pregnant mice can be passed on to prenatal and postnatal mice through amniotic fluid and breast milk. This may in turn influence the sweet preference of the growing mice. (10,11,12)
One of the questions I’m frequently asked is whether natural, non-nutritive sweeteners such as stevia have a similar affect as artificial counterparts. The limited amount of data available indicates otherwise. A head-to-head study from August 2010 pitted aspartame against stevia in a group of 31 adults. Before and after blood tests revealed that stevia demonstrated a milder influence on blood sugar and insulin than aspartame. It’s also important to note that while aspartame is often associated with adverse effects in clinical trials, stevia is typically linked to “side benefits” including anti-diabetic activity, i.e. protection against kidney and pancreatic beta-cell damage. (13,14,15)
If you examine the labels of many stevia-based sweeteners you’ll notice that they often contain “other ingredients”. These natural substances are typically used as carriers. Pure stevia is extremely sweet, purportedly up to 300 times as sweet as common table sugar. Therefore, it needs to be diluted by adding it to a much less sweet base ingredient. Erythritol and inulin are two of the most commonly used additives in stevia products. The good news about these supporting ingredients is that they also have side benefits of their own. Erythritol possesses potent antioxidant properties that may shield the cardiovascular system from elevated blood sugar or hyperglycemia. Inulin is a prized prebiotic that supports the growth of healthy bacteria in the gut in both old and young alike. It is for these reasons that I tend to use stevia and stevia blends in the Heathy Fellow test kitchen instead of artificial sweeteners. After reading today’s column, I hope you’ll consider doing the same. (16,17,18)
Note: Please check out the “Comments & Updates” section of this blog – at the bottom of the page. You can find the latest research about this topic there!
Tags: Erythritol, Inulin, Stevia, Sugar
Posted in Diet and Weight Loss, Food and Drink, Nutrition
June 30th, 2011 at 7:26 am
As a former diet cola drinker, I’ve been following the aspartame issue with great interest and skepticism. It does seem that some of the studies involving aspartame are still at the preliminary level (not controlled, human trials). I recall hearing about how some people exaggerated one preliminary trial in mice to say that aspartame causes cancer (or some nonsense).
However, I stopped drinking diet cola partly because I wanted to reduce the amount of caffeine and sodium, but also because I think there are several independent studies going on that will see if there is a link between aspartame and diabetes – and since diabetes runs in my family, I thought it’d be good idea to stop drinking it all together.
Good tip on the Stevia, JP. What’s your take on splenda? I noticed you’ve written about it before, but nothing too new (unless I’ve missed it). Any updates on research involving splenda?
June 30th, 2011 at 12:29 pm
Most of the data on sucralose presents a relatively acceptable safety profile, IMO. However, I’m still concerned about the long term effects. Also, the addition of maltodextrin to sucralose probably isn’t the best idea.
My wife tends to prefer the taste of sucralose over stevia in some products and recipes. I do my best to find ways of encouraging her to switch over (to stevia) – sometimes successfully. I just made a stevia sweetened batch of brownies which she enjoyed. Also, we’re currently eating a coconut milk ice cream that is partially sweetened with stevia.
The good news: http://www.sciencedirect.com/science/article/pii/S0278691510005053
The bad news: http://www.nature.com/ejcn/journal/v65/n4/full/ejcn2010291a.html
Note: Splenda and similar sucralose-based sweeteners tend to use maltodextrin as a base ingredient.
June 30th, 2011 at 9:48 pm
Nice one, JP!
July 1st, 2011 at 12:04 pm
Thank you, Orna! 🙂
October 31st, 2011 at 2:41 pm
I have a question for you…I have been drinking Iced tea from TJ’s, it contains cane syrup solids, instant tea, Maltodextrin, Citric Acid, natural lemon flavor, contains less than 2% of the following: Stevia extract, (Rebaudioside A) salt, Magnesium oxide, silicon dioxide…
!5 cals./8 oz. 0fat, 20mg sodium, total cabs 4 g, sugars3, protein 0,
I do not drink soda and have not for many years…I like Iced tea some afternoons, I may have 2 glasses a few times a week…
What are your thoughts on this…I do not want to gain weight..
Hope you have been well
October 31st, 2011 at 5:43 pm
I doubt this low-cal iced tea will be problematic … in the context of an otherwise healthy diet. Have you noticed any change in your weight since using this product? If you happen to have a blood sugar monitor, you can test to see how your body reacts to it. I often do this when experimenting with new products or recipes. I’m a big believer in personal detective work (testing blood sugar, watching the scale, etc.) because individual reactions can vary significantly.
October 31st, 2011 at 11:11 pm
JP, Thank you so much! No, I have not noticed any weight gain at all.I saw Cane Syrup and thought, oh my this will make me put on the pounds.That is an excellent idea using a Glucometer, never thought of doing that to see the possible rise.
I love your web site and use things often, like eating an apple for reflux, works like a charm.
Once again I thank you JP,
November 1st, 2011 at 4:03 pm
Thank you for your kind comments. I appreciate it! 🙂
A small amount of cane sugar is unlikely to be the downfall of most low carb diets. Fructose is a worse offender, IMO. But, in both cases, “dose makes the poison”. The body can usually handle small amounts of unhealthy ingredients in the context of an otherwise nutrient dense diet. In other words … don’t sweat the small stuff.
November 10th, 2011 at 5:54 pm
Do you know of any research being done on how sweeteners affect the nervous system? Diabetics know that sweeteners destroy the myelin sheaths of nerves, causing first pain, then numbness, injury, gangrene, and loss of fingers, toes and even legs and arms. What is to stop sweeteners from affecting other nerves, including the nerves in the brain, in the spine, and which transmit instructions to muscles? I believe sweeteners may be contributing causes of such diseases as dystonia, dementia, Altzheimer’s and Parkinson’s. Any disease or condition which may include nerves could be affected by sweeteners attacking the nerves. Any info on that???
November 11th, 2011 at 4:11 pm
I’m not aware of any evidence linking natural, sugar-alternatives with nerve damage. My favorite sweeteners tend to have a minimal/negligible impact on blood sugar and insulin. They also possess antioxidant properties which likely protect the nervous system to some degree.
May 13th, 2015 at 9:01 pm
Nature. 2014 Oct 9;514(7521):181-6.
Artificial sweeteners induce glucose intolerance by altering the gut microbiota.
Non-caloric artificial sweeteners (NAS) are among the most widely used food additives worldwide, regularly consumed by lean and obese individuals alike. NAS consumption is considered safe and beneficial owing to their low caloric content, yet supporting scientific data remain sparse and controversial. Here we demonstrate that consumption of commonly used NAS formulations drives the development of glucose intolerance through induction of compositional and functional alterations to the intestinal microbiota. These NAS-mediated deleterious metabolic effects are abrogated by antibiotic treatment, and are fully transferrable to germ-free mice upon faecal transplantation of microbiota configurations from NAS-consuming mice, or of microbiota anaerobically incubated in the presence of NAS. We identify NAS-altered microbial metabolic pathways that are linked to host susceptibility to metabolic disease, and demonstrate similar NAS-induced dysbiosis and glucose intolerance in healthy human subjects. Collectively, our results link NAS consumption, dysbiosis and metabolic abnormalities, thereby calling for a reassessment of massive NAS usage.
July 12th, 2015 at 12:33 pm
Environ Sci Technol. 2014 Dec 2;48(23):13668-74.
Fate of artificial sweeteners in wastewater treatment plants in New York State, U.S.A.
Very few studies describe the fate of artificial sweeteners (ASWs) in wastewater treatment plants (WWTPs). In this study, mass loadings, removal efficiencies, and environmental emission of sucralose, saccharin, aspartame, and acesulfame were determined based on the concentrations measured in wastewater influent, primary effluent, effluent, suspended particulate matter (SPM), and sludge collected from two WWTPs in the Albany area of New York State, U.S.A. All ASWs were detected at a mean concentration that ranged from 0.13 (aspartame) to 29.4 μg/L (sucralose) in wastewater influent, 0.49 (aspartame) to 27.7 μg/L (sucralose) in primary influent, 0.11 (aspartame) to 29.6 μg/L (sucralose) in effluent, and from 0.08 (aspartame) to 0.65 μg/g dw (sucralose) in sludge. Aspartame was found in 92% of influent SPM samples at a mean concentration of 444 ng/g dw, followed by acesulfame (92 ng/g) and saccharin (49 ng/g). The fraction of the total mass of ASWs sorbed to SPM was in the rank order: aspartame (50.4%) > acesulfame (10.9%) > saccharin and sucralose (0.8%). The sorption coefficients of ASWs ranged from 4.10 (saccharin) to 4540 L/kg (aspartame). Significant removal of aspartame (68.2%) and saccharin (90.3%) was found in WWTPs; however, sucralose and acesulfame were less efficiently removed (<2.0%). The total mass loading of sucralose, saccharin, and acesulfame in the WWTP that served a smaller population (∼15,000) was 1.3-1.5 times lower than that in another WWTP that served a larger population (∼100,000). The average daily loading of sucralose in both WWTPs (18.5 g/d/1000 people) was ∼2 times higher than the average loading of saccharin. The daily discharge of sucralose from the WWTPs was the highest (17.6 g/d/1000 people), followed by acesulfame (1.22 g/d/1000 people), and saccharin (1.07 g/d/1000 people). Approximately, 1180 g of saccharin and 291 g of acesulfame were transformed in or removed daily from the two WWTPs. This is the first study to describe the fate of ASWs, including the fraction found in SPM and in sludge, in addition to the aqueous portion of wastewater in WWTPs.
July 12th, 2015 at 12:38 pm
Int J Clin Exp Med. 2015 Apr 15;8(4):6133-44. eCollection 2015.
Alterations in lipid profile, oxidative stress and hepatic function in rat fed with saccharin and methyl-salicylates.
BACKGROUND: Food additives attract consumers, improve foods quality, control weight, and replace sugar in foods, while it may affect seriously children and adults health.
AIM: To investigate the adverse effects of saccharin and methylsalicyltaes on lipid profile, blood glucose, renal, hepatic function, and oxidative stress/antioxidant (lipid peroxidation, Catalase and reduced glutathione (GSH) in liver tissues).
METHODS: 46 young male albino rats were used. Saccharin and methylsalicylate were giving orally as low and high dose for 30 days. Rats were divided into 5 groups, 1(st) control group, 2(nd) and 3(rd) low and high saccharin-treated groups and 4(th) and 5(th) low and high methylsalicylate-treated group.
RESULTS: Serum total cholesterol, triglyceride, glucose levels and body weight gain were decreased in saccharin high dose compared to control. Rats ingested high dose of saccharin presented a significant reduction in serum triglycerides, cholesterol and LDL levels. Low and high doses of saccharin exhibited a significant increase in liver function marker of ALT, AST, ALP activity, total proteins and albumin levels and renal function test (urea and creatinine levels) in comparison with control group. Saccharin high dose induce a significant decline in hepatic GSH levels, catalase and SOD activities while increased in hepatic MDA level.
CONCLUSION: It could be concluded that, saccharin affects harmfully and alters biochemical markers in hepatic and renal tissues not only at greater doses but also at low doses. Whereas uses of metylsalicylates would not pose a risk for renal function and hepatic oxidative markers.
July 12th, 2015 at 12:49 pm
Int J Food Sci Nutr. 2015 May 26:1-6.
Study of Stevia rebaudiana Bertoni antioxidant activities and cellular properties.
The aim of our study was to determine the antioxidant activities, cytotoxicity and proliferative properties in Stevia rebaudiana leaves and stems. Leaves extracts exhibited a higher antioxidant activity than stems extract, through oxygen radical absorbance capacity (ORAC) and cellular antioxidant activity (CAA) assays. Stevioside and rebaudioside A, the main sweetening metabolites in stevia leaves, exhibited a low ORAC value in comparison with plant extracts, while did not elicit any CAA. Stevia rebaudiana did not exhibit toxicity against HepG2 (hepatocellular carcinoma) human cells. No proliferative nor catalase modulations were observed in cells treated with such extracts. Our findings support the promising role of stevia that, apart from its sweetness, can act as a source of antioxidants, even at the intracellular level. This activity makes S. rebaudiana crude extract an interesting resource of natural sweetness with antioxidant properties which may find numerous applications in foods and nutritional supplements industries.
December 6th, 2015 at 4:52 pm
Appetite. 2015 Nov 7;96:604-610.
Sweet taste of saccharin induces weight gain without increasing caloric intake, not related to insulin-resistance in Wistar rats.
In a previous study, we showed that saccharin can induce weight gain when compared with sucrose in Wistar rats despite similar total caloric intake. We now question whether it could be due to the sweet taste of saccharin per se. We also aimed to address if this weight gain is associated with insulin-resistance and to increases in gut peptides such as leptin and PYY in the fasting state. In a 14 week experiment, 16 male Wistar rats received either saccharin-sweetened yogurt or non-sweetened yogurt daily in addition to chow and water ad lib. We measured daily food intake and weight gain weekly. At the end of the experiment, we evaluated fasting leptin, glucose, insulin, PYY and determined insulin resistance through HOMA-IR. Cumulative weight gain and food intake were evaluated through linear mixed models. Results showed that saccharin induced greater weight gain when compared with non-sweetened control (p = 0.027) despite a similar total caloric intake. There were no differences in HOMA-IR, fasting leptin or PYY levels between groups. We conclude that saccharin sweet taste can induce mild weight gain in Wistar rats without increasing total caloric intake. This weight gain was not related with insulin-resistance nor changes in fasting leptin or PYY in Wistar rats.
December 20th, 2015 at 9:33 pm
J Hypertens. 2015 Dec 16.
Soft drink consumption, mainly diet ones, is associated with increased blood pressure in adolescents.
OBJECTIVE: The aim of this cross-sectional study was to investigate the association between consumption of sugar-sweetened and diet soft drinks with blood pressure (BP) in adolescents.
METHODS: Fifth graders of 20 public schools were invited to participate in an intervention aimed at behavioral dietary changes and had their BP, weight, and height measured at baseline. Type and frequency of soft drink consumption were assessed using a food and beverages frequency questionnaire, and students were classified as nonconsumers, sugar-sweetened soft drink consumers, and diet soft drink consumers.
RESULTS: Of the 574 students invited, 512 were examined and 488 had their BP measured. Of these, 25 (5.1%) reported to be nonconsumers, 419 (85.9%) were sugar-sweetened soft drink consumers, and 44 (9%) were diet soft drink consumers. Mean SBP and DBP were 101.3/57.8, 102.6/58.8, and 106.0/61.3 mmHg for these three groups of consumption, respectively. After adjustment for sex, age, BMI, physical activity, addition of salt to food, and education of the head of the family, SBP was 5.4 mmHg higher in the diet soft drink consumers group compared with the nonconsumers group and 3.3 mmHg higher compared with the sugar-sweetened consumers group (P value of trend = 0.01). Moreover, DBP was also higher among diet soft drink consumers compared with nonconsumers, with a difference of 3.3 mmHg, and compared with sugar-sweetened consumers, with a difference of 2.3 mmHg (P value of trend = 0.04).
CONCLUSION: The results indicate that the consumption of soft drink is associated with increased BP, which is further increased by drinking diet type sodas.
November 29th, 2016 at 7:05 pm
PLoS One. 2016 Nov 23;11(11):e0167241.
Chronic Low-Calorie Sweetener Use and Risk of Abdominal Obesity among Older Adults: A Cohort Study.
INTRODUCTION: Low-calorie sweetener use for weight control has come under increasing scrutiny as obesity, especially abdominal obesity, remain entrenched despite substantial low-calorie sweetener use. We evaluated whether chronic low-calorie sweetener use is a risk factor for abdominal obesity.
PARTICIPANTS AND METHODS: We used 8268 anthropometric measurements and 3096 food diary records with detailed information on low-calorie sweetener consumption in all food products, from 1454 participants (741 men, 713 women) in the Baltimore Longitudinal Study of Aging collected from 1984 to 2012 with median follow-up of 10 years (range: 0-28 years). At baseline, 785 were low-calorie sweetener non-users (51.7% men) and 669 participants were low-calorie sweetener users (50.1% men). Time-varying low-calorie sweetener use was operationalized as the proportion of visits since baseline at which low-calorie sweetener use was reported. We used marginal structural models to determine the association between baseline and time-varying low-calorie sweetener use with longitudinal outcomes-body mass index, waist circumference, obesity and abdominal obesity-with outcome status assessed at the visit following low-calorie sweetener ascertainment to minimize the potential for reverse causality. All models were adjusted for year of visit, age, sex, age by sex interaction, race, current smoking status, dietary intake (caffeine, fructose, protein, carbohydrate, and fat), physical activity, diabetes status, and Dietary Approaches to Stop Hypertension score as confounders.
RESULTS: With median follow-up of 10 years, low-calorie sweetener users had 0.80 kg/m2 higher body mass index (95% confidence interval [CI], 0.17-1.44), 2.6 cm larger waist circumference (95% CI, 0.71-4.39), 36.7% higher prevalence (prevalence ratio = 1.37; 95% CI, 1.10-1.69) and 53% higher incidence (hazard ratio = 1.53; 95% CI 1.10-2.12) of abdominal obesity than low-calorie sweetener non-users.
CONCLUSIONS: Low-calorie sweetener use is independently associated with heavier relative weight, a larger waist, and a higher prevalence and incidence of abdominal obesity suggesting that low-calorie sweetener use may not be an effective means of weight control.
December 20th, 2016 at 5:02 pm
Int J Obes (Lond). 2016 Dec 13.
Effects of aspartame-, monk fruit-, Stevia-, and sucrose-sweetened beverages on postprandial glucose, insulin and energy intake.
BackgroundSubstituting sweeteners with non-nutritive sweeteners (NNS) may aid in glycaemic control and body weight management. Limited studies have investigated energy compensation, glycaemic and insulinaemic responses to artificial and natural NNS.ObjectivesThis study compared the effects of consuming NNS (artificial vs. natural) and sucrose (65 g) on energy intake, blood glucose and insulin responses.MethodsThirty healthy males took part in this randomised, crossover study with four treatments: aspartame-, monk fruit-, Stevia-, and sucrose-sweetened beverages. On each test day, participants were asked to consume a standardised breakfast in the morning and they were provided with test beverage as a preload in mid-morning and ad libitum lunch was provided an hour after test beverage consumption. Blood glucose and insulin concentrations were measured every 15 min within the first hour of preload consumption and every 30 min for the subsequent two hours. Participants left the study site three hours after preload consumption and completed a food diary for the rest of the day.ResultsAd libitum lunch intake was significantly higher for the NNS treatments compared to sucrose (P=0.010). The energy “saved” from replacing sucrose with NNS was fully compensated for at subsequent meals, hence no difference in total daily energy intake was found between the treatments (P=0.831). The sucrose-sweetened beverage led to large spikes in blood glucose and insulin responses within the first hour whereas these responses were higher for all three NNS beverages following the test lunch. Thus, there were no differences in total area under the curve (AUC) for glucose (P=0.960) and insulin (P=0.216) over three hours between the four test beverages.ConclusionsThe consumption of calorie free beverages sweetened with artificial and natural NNS have minimal influences on total daily energy intake, postprandial glucose and insulin compared to a sucrose-sweetened beverage.
May 29th, 2017 at 12:18 pm
Food Chem. 2017 Oct 1;232:379-386.
Antioxidant activities of aqueous extract from Stevia rebaudiana stem waste to inhibit fish oil oxidation and identification of its phenolic compounds.
We investigated the potential for exploiting Stevia rebaudiana stem (SRS) waste as a source of edible plant-based antioxidants finding for the first time that the hot water extract of SRS had significantly higher antioxidant activity against fish oil oxidation than that of the leaf, despite SRS extract having lower total phenolic content, DPPH radical scavenging activity and ORAC values. To locate the major antioxidant ingredients, SRS extract was fractionated using liquid chromatography. Five phenolic compounds (primary antioxidant components in activity-containing fractions) were identified by NMR and HR-ESI-MS: vanillic acid 4-O-β-d-glucopyranoside (1), protocatechuic acid (2), caffeic acid (3), chlorogenic acid (4) and cryptochlorogenic acid (5). Further analysis showed that, among compounds 2-5, protocatechuic acid had the highest capacity to inhibit peroxides formation, but exhibited the lowest antioxidant activities in DPPH and ORAC assays. These results indicate that SRS waste can be used as strong natural antioxidant materials in the food industry.
June 11th, 2017 at 4:12 pm
PLoS One. 2017 Jun 8;12(6):e0178426.
The artificial sweetener acesulfame potassium affects the gut microbiome and body weight gain in CD-1 mice.
Artificial sweeteners have been widely used in the modern diet, and their observed effects on human health have been inconsistent, with both beneficial and adverse outcomes reported. Obesity and type 2 diabetes have dramatically increased in the U.S. and other countries over the last two decades. Numerous studies have indicated an important role of the gut microbiome in body weight control and glucose metabolism and regulation. Interestingly, the artificial sweetener saccharin could alter gut microbiota and induce glucose intolerance, raising questions about the contribution of artificial sweeteners to the global epidemic of obesity and diabetes. Acesulfame-potassium (Ace-K), a FDA-approved artificial sweetener, is commonly used, but its toxicity data reported to date are considered inadequate. In particular, the functional impact of Ace-K on the gut microbiome is largely unknown. In this study, we explored the effects of Ace-K on the gut microbiome and the changes in fecal metabolic profiles using 16S rRNA sequencing and gas chromatography-mass spectrometry (GC-MS) metabolomics. We found that Ace-K consumption perturbed the gut microbiome of CD-1 mice after a 4-week treatment. The observed body weight gain, shifts in the gut bacterial community composition, enrichment of functional bacterial genes related to energy metabolism, and fecal metabolomic changes were highly gender-specific, with differential effects observed for males and females. In particular, ace-K increased body weight gain of male but not female mice. Collectively, our results may provide a novel understanding of the interaction between artificial sweeteners and the gut microbiome, as well as the potential role of this interaction in the development of obesity and the associated chronic inflammation.
July 8th, 2018 at 6:02 pm
PLoS One. 2018 Jul 5;13(7):e0199080.
Non-nutritive sweeteners possess a bacteriostatic effect and alter gut microbiota in mice.
Non-nutritive sweeteners (NNSs) are widely used in various food products and soft drinks. There is growing evidence that NNSs contribute to metabolic dysfunction and can affect body weight, glucose tolerance, appetite, and taste sensitivity. Several NNSs have also been shown to have major impacts on bacterial growth both in vitro and in vivo. Here we studied the effects of various NNSs on the growth of the intestinal bacterium, E. coli, as well as the gut bacterial phyla Bacteroidetes and Firmicutes, the balance between which is associated with gut health. We found that the synthetic sweeteners acesulfame potassium, saccharin and sucralose all exerted strong bacteriostatic effects. We found that rebaudioside A, the active ingredient in the natural NNS stevia, also had similar bacteriostatic properties, and the bacteriostatic effects of NNSs varied among different Escherichia coli strains. In mice fed a chow diet, sucralose increased Firmicutes, and we observed a synergistic effect on Firmicutes when sucralose was provided in the context of a high-fat diet. In summary, our data show that NNSs have direct bacteriostatic effects and can change the intestinal microbiota in vivo.