ARTIFICIAL SWEETENERS

“Natural” does not necessarily mean healthy. Remember, table sugar is natural too. We intuitively suspect that natural ingredients are more likely to be well tolerated by the body and to not have unexpected, detrimental health consequences. Many artificial compounds have unexpected interactions with our complex biology. Here is a list of synthetic sweeteners and evidence that led us to avoid them. Some are reasonably safe to consume in reasonable quantities, but why consume them if we can enjoy natural and healthy sweet ingredients instead?

Most Common ARTIFICIAL Sweeteners and WHY we AVOID them

Maltitol

This is the MOST COMMON sweetening ingredient in ‘sugar-free’ chocolate. WHY? Because it tastes like sugar, feels like sugar, and behaves like sugar. Food companies love it for this, coupled with the fact that they can state that the product has 0g / 100g sugar. Maltitol has c. 2.8-3.5 calories per gram, similar to sugar (4 kcal/g). It is metabolized into sorbitol and glucose. Sorbitol in turn is metabolized into fructose. Sound familiar? Glucose + Fructose = Sucrose (Sugar).

WHY AVOID?

MOST IMPORTANTLY, maltitol in humans is largely absorbed by the small intestine and it breaks down into SORBITOL (which breaks down to fructose + glucose) + glucose, the very monosaccharides that comprise SUCROSE (iv, v, vi). Sugar-free on the label, SUGAR INSIDE the body. What is not absorbed by the small intestine is fermented by colonic bacteria, and there is insufficient research yet on whether or not it has a detrimental effect therein.

Maltitol is HIGHLY LAXATIVE. Even a dose of 20g in adults causes flatulence, bloating, stomach pain, and diarrhea (ii). Most maltitol-sweetened sugar-free chocolates contain > 40g/100g. The sweetest maltitol chocolates usually are 50% maltitol by weight, so you may eat this amount in one sitting.

There is NO RELEVANT CALORIE SAVING when switching from SUGAR to MALTITOL (iii, iv).

During pregnancy, maltitol may cause HYPERGLYCEMIA and be embryotoxic, causing low embryonic weight at doses of even just 1g/kg body weight (a physiologic amount one might consume) (vii).

(i) Nabors, L.O. (2001) ‘Alternative Sweeteners, Third Edition, Revised and Expanded’, Marcel Dekker, Inc., p. 250

(ii) Koizumi, N. et al. (1982) ‘Studies on transitory laxative effects of sorbitol and maltitol: II: Differences in laxative effects among various foods containing the sweetening agents’, Chemosphere, 12(1), pp. 105-116

(iii) Kruger, D. et al. (1992) ‘Gastrointestinal transit and digestibility of maltitol, sucrose and sorbitol in rats: A multicompartmental model and recovery study’, Experientia, 48

(iv) Beaugerie, L. et al. (1990) ‘Digestion and Absorption in the Human Intestine of Three Sugar Alcohols’, Gastroenterology, 99(3), pp. 717-723

(v) Wursch, P. et al. (1990) ‘Metabolism of maltitol by conventional rats and mice and germfree mice, and comparative digestibility between maltitol and sorbitol in germ-free mice’, British Journal of Nutrition, 63, pp. 7-15

(vi) Lian-Loh, R. et al. (1982), ’The metabolism of maltitol in the rat’, British Journal of Nutrition, 48, p. 477

(vii) Canimoglu, S. and Rencuzogullari, E. (2012) ‘The genotoxic and teratogenic effects of maltitol in rats’, Toxicology and Industrial Health, 29(10), pp. 935-943

Isomalt

Isomalt breaks down into glucose (50%), sorbitol (25%) and mannitol (25%) (i). Mannitol is – like sorbitol – metabolized into fructose. It has c. 2kcal/g.

WHY AVOID?

Isomalt is a LAXATIVE and causes borborygmi, colic, stomach-ache, bloating, and flatulence at doses of 25g-40g (ii, iii, iv).

Isomalt breaks down partly into sorbitol and mannitol, both of which break down into FRUCTOSE. If you want to avoid fructose, this artificial sweetener does not help you to.

Isomalt promotes gas (400% more than sucrose) (iv).

(i) Goldstein, D. (2015) ‘The Oxford Companion to Sugar and Sweets’, Oxford University Press

(ii) Lee, A. et al. (2002) ‘The comparative gastrointestinal responses of children and adults following consumption of sweets formulated with sucrose, isomalt and lycasin HBC’, Eur J Clin Nutr., 56(8), pp. 755-64

(iii) Kotsou, G.A. et al. (1996), ‘Dose-related gastrointestinal response to the ingestion of either isomalt, lactitol or maltitol in milk chocolate’, Eur J Clin Nutr., 50(1), pp. 17-21

(iv) Lee, A. et al. (1994) ‘Breath hydrogen after ingestion of the bulk sweeteners sorbitol, isomalt and sucrose in chocolate’, British Journal of Nutrition 71(5), pp. 731-737

Sorbitol

Thankfully, this sweetener is less often used in chocolate and food products these days, mainly due to its highly laxative effect, but you will still find it in some products. It is metabolized to fructose. What is so paradoxical about sorbitol as a choice away from sugar, is that it feeds into a pathway that is directly associated with diabetes: the polyol pathway that generates fructose and creates reactive oxygen species, mitochondrial dysfunction, and advanced glycation end products (AGEs) (i).

WHY AVOID?

Sorbitol is metabolized into glucose and fructose, i.e. sugar. This does not help those aiming to avoid sugar.

Sorbitol is HIGHLY LAXATIVE. Even a dose of 10g in an adult causes flatulence, bloating, stomach pain and diarrhea (ii). Most sorbitol-sweetened sugar-free chocolate bars contain > 40g/100g.

There is NO CALORIE SAVING when switching from SUGAR to SORBITOL (iii, iv).

Sorbitol’s conversion to fructose leads to MITOCHONDRIAL DYSFUNCTION (i).

Sorbitol’s conversion to fructose leads to INFLAMMATION, AGEing and DIABETIC COMPLICATIONS from retinopathy to nephropathy (i, v, vi, vii, viii).

Sorbitol is metabolized by: E. coli, Salmonella and Shigella, bacterial species that are associated with pathology (ix, x).

(i) Tang, W.H. et al. (2012) ‘Aldose reductase, oxidative stress, and diabetic mellitus’, Frontiers in Pharmacology, 3(87)

(ii) Koizumi, N. et al. (1982) ‘Studies on transitory laxative effects of sorbitol and maltitol: II: Differences in laxative effects among various foods containing the sweetening agents’, Chemosphere, 12(1), pp. 105-116

(iii) Kruger, D. et al. (1992) ‘Gastrointestinal transit and digestibility of maltitol, sucrose and sorbitol in rats: A multicompartmental model and recovery study’, Experientia, 48

(iv) Beaugerie, L. et al. (1990) ‘Digestion and Absorption in the Human Intestine of Three Sugar Alcohols’, Gastroenterology, 99(3), pp. 717-723

(v) Friedman, E.A. (1999) ‘Advanced glycosylated end products and hyperglycemia in the pathogenesis of diabetic complications’, Diabetes Care, 22(2), pp. B65-71

(vi) Lorenzi, M. and Oates, P.J. (2008) ‘The Polyol Pathway and Diabetic Retinopathy’, Contemporary Diabetes: Diabetic Retinopathy, Humanah Press, Totowa, NJ.

(vii) Bjornstad, P. et al. (2015) ’Fructose and uric acid in diabetic nephropathy’, Diabetologia, 58(9), pp. 1993-2002.

(viii) Julius U. et al. (2008) ‘Sorbitol Pathway of Glucose Metabolism and Dyslipidemia’, 77th Congress of the European Atherosclerosis Society, PO6-40

(ix) Lee, A. et al. (1994) ‘Breath hydrogen after ingestion of the bulk sweeteners sorbitol, isomalt and sucrose in chocolate’, British Journal of Nutrition 71(5), pp. 731-737

(x) Payne, A.N. et al. (2012) ‘Gut microbial adaptation to dietary consumption of fructose, artificial sweeteners and sugar alcohols: implications for host–microbe interactions contributing to obesity’, Obesity Reviews, 13, pp. 799-809

Acesulfame K (Ace-K)

Ace-K is an artificial sweetener with a slightly bitter aftertaste, so you will often find it in combination with other artificial sweeteners. It is common in artificially-sweetened drinks.

WHY AVOID?

Ace-K has been shown to cause WEIGHT GAIN in animal studies, albeit at >double the dose one might expect to consume in one day. These same studies also observed epigenetic changes in energy metabolism genes which provide a possible explanation for the weight gain (i, vi).

Ace-K increased INFLAMMATORY endotoxin lipopolysaccharide (LPS) synthesis genes significantly and the synthesis gene for a bacterial toxin that is a VIRULENCE factor that stimulates the inflammatory mediators including CYTOKINES (i).

Ace-K appears to increase GLUCOSE RESPONSES and raise insulin. In those with insulin resistance, this may increase cardiovascular disease risk (v, vi).

Ace-K INCREASES GLUCOSE RESPONSES and STIMULATES INCRETIN secretion, which RAISES INSULIN. In those with insulin resistance or metabolic syndrome, this may increase cardiovascular disease risk (v, vi).

Ace-K may directly stimulate ADIPOGENESIS and suppress LIPOLYSIS, leading to FAT GAIN and increasing the risk of ATHEROSCLEROSIS (CVD) (vii, viii).

Chronic Ace-K intake may increase the risk of cognitive impairment (ix).

(i) Bian, X. et al. (2017) ‘The artificial sweetener acesulfame potassium affects the gut microbiome and body weight gain in CD-1 mice’, PLOS ONE, 12(6)

(ii) Karstadt, M.L. (2009) ‘Regulation of carcinogenic food additives in the United States’, Eur. J. Oncol., 14(2), pp. 79-92

(iii) Bloomgarden, Z.T. (2010 ‘Nonnutritive Sweeteners, Fructose, and Other Aspects of Diet’, Diabetes Care, 34

(iv) Karstadt, M.L. (2009) ‘Testing Needed for Acesulfame Potassium, an Artificial Sweetener’, Environ Health Perspect. 114(9)

(v) Chan, C. et al. (2017) ‘The impact of low and no-caloric sweeteners on glucose absorption, incretin secretion and glucose tolerance’, Applied Physiology, Nutrition and Metabolism

(vi) Yamaoka-Tojo, M. (2010) ‘Elevated circulating levels of an incretin hormone, glucagon-like peptide-1, are associated with metabolic components in high-risk patients with cardiovascular disease’, Cardiovascular Diabetology, 9(17)

(vii) Lin, CH. et al (2021), ‘Consumption of Non-Nutritive Sweetener, Acesulfame Potassium Exacerbates Atherosclerosis through Dysregulation of Lipid Metabolism in ApoE-/- Mice’, Nutrients. 2021 Nov 9;13(11):3984.

(viii) Simon, B.R. (2013) ‘Artificial Sweeteners Stimulate Adipogenesis and Suppress Lipolysis Independently of Sweet Taste Receptors’, The Journal of Biological Chemistry, 288, pp. 32475-32489

(ix) Cong, W-n. (2013) ‘Long-Term Artificial Sweetener Acesulfame Potassium Treatment Alters Neurometabolic Functions in C57BL/6J Mice’, PLOS ONE, 8(8)

Aspartame & Neotame

Aspartame is an artificial sweetener that breaks down into aspartic acid, phenylalanine, and methanol. Products containing it must provide a warning label for phenylketonuria patients. Methanol is further broken down into formaldehyde. There are thousands of studies on the independent, adverse health impacts of excessive aspartic acid, phenylalanine, and methanol.

NEOTAME is made from ASPARTAME and is very similar structurally. Because neotame is 7,000-13,000x sweeter vs. SUGAR, it can be used in tiny quantities and be HIDDEN in the words “flavors” or “flavoring” on food labels.

WHY AVOID?

KEY: most aspartame studies have been performed on rats, which hydroxylate (transform) aspartame 5x faster than humans, so studies on rats using the acceptable daily intake (ADI) of 40mg/kg body weight for humans, might show benign results, yet show adverse impacts at 200mg/kg body weight, which might be the relevant-to-human dose (i).

Even at lower than the ADI for humans, aspartame consumption may generate carcinogenic effects and be directly cytotoxic (ii, iii). Epidemiological studies are not conclusive as to whether aspartame is carcinogenic.

Aspartame appears to cause cardiac oxidative stress in animals, even at levels deemed safe by regulators (iv).

Aspartame causes NEUROBEHAVIOURAL changes and negatively impacts mood, increasing IRRITABILITY and DEPRESSION (v). The mechanisms by which aspartame causes this include: disturbed amino acid (protein) metabolism, neuronal dysfunction and hormonal imbalances, neurotransmitter changes that impact serotonin regulation (vi).

Aspartame’s breakdown products may cause DNA damage and abnormal brain development so should be AVOIDED during PREGNANCY (vii).

Aspartame and its breakdown products may cause MITOCHONDRIAL dysfunction, which leads to impaired FAT METABOLISM and impaired GABA production, which directly disrupts mood (viii).

Aspartame may create permeability and compromise the blood-brain barrier, promoting NEURODEGENERATION (viii, ix).

Aspartame may cause adverse microbiome changes, with increases in bacteria associated with pathology (x).

Aspartame may lead to higher fasting glucose and insulin resistance in those with obesity (xi). Aspartame appears to promote significant fat gain, including liver fat, and insulin resistance in animal models (xii).

(i) Fernstrom, J.D. (1989) ‘Oral aspartame and plasma phenylalanine: pharmacokinetic difference between rodents and man, and relevance to CNS effects of phenylalanine’, Journal of Neural Transmission, 75, pp. 159-164

(ii) Soffritti, M. et al. (2006) ’ First Experimental Demonstration of the Multipotential Carcinogenic Effects of Aspartame Administered in the Feed to Sprague-Dawley Rats’, Environmental Health Perspectives, 114(3), pp. 379-385

(iii) Maghiari, A. L. et al. (2020) ‘High Concentrations of Aspartame Induce Pro-Angiogenic Effects in Ovo and Cytotoxic Effects in HT-29 Human Colorectal Carcinoma Cells’, Nutrients, 2020, 12, p. 3600

(iv) Choudhary, A.K. et al. (2015) ‘Aspartame induced cardiac oxidative stress in Wistar albino rats’, Nutrition clinique et metabolisme, 30, pp. 29-37

(v) Lindseth, G.N. et al. (2014) ‘Neurobehavioral Effects of Aspartame Consumption’, Res Nurs Health, 37(3), pp. 185-193

(vi) Choudhary, A.K. (2018) ‘The debate over neurotransmitter interaction in aspartame usage’, Journal of Clinical Neuroscience, 56, pp. 7-15.

(vii) Manabe, S. et al. (1993), ‘Effect of excess phenylalanine diet during pregnancy on fetal brain growth in rats. Tokushima J Exp Med., 40(3-4), pp. 125-35.

(viii) Humphries, P. et al. (2008), ‘Direct and indirect cellular effects of aspartame on the brain’, 62, pp. 451-62.

(ix) Choudhary AK, Lee YY. The debate over neurotransmitter interaction in aspartame usage. J Clin Neurosci. 2018 Oct;56:7-15.

(x) Palmnäs, M.S.A. et al. (2014), ‘Low-Dose Aspartame Consumption Differentially Affects Gut Microbiota-Host Metabolic Interactions in the Diet-Induced Obese Rat’, PLOS ONE, 9(10).

(x) Kuk, J.L. and Brown, R.E. (2016) ‘Aspartame intake is associated with greater glucose intolerance in individuals with obesity’ Appl Physiol Nutr Metab., 41(7), pp. 795-8.

(xi) Doueihy, NE. et al (2025), ‘Aspartame and Human Health: A Mini-Review of Carcinogenic and Systemic Effects’, J Xenobiot. 2025 Jul 7;15(4):114.

(xii) Ragi M-EE et al (2022), ‘The effect of aspartame and sucralose intake on body weight measures and blood metabolites: role of their form (solid and/or liquid) of ingestion. British Journal of Nutrition’, 2022;128(2):352-360.

Saccharin

Saccharin (a.k.a. benzoic sulfimide) is an artificial sweetener with a metallic aftertaste at high concentrations.

WHY AVOID?

Saccharin reduces plasma antioxidants and generates OXIDATIVE STRESS and excess reactive-oxygen species (ROS). It increases lipid peroxidation and secondary oxidants and DNA-reactive aldehydes that may lead to DNA damage (i, ii).

Saccharin causes changes that indicate LIVER DYSFUNCTION, including (but not only) significantly increased alkaline phosphatase, a biomarker associated with LIVER DISEASE (i, ii).

Saccharin causes OVEREXPRESSION of a key ONCOGENE and DOWNREGULATION of a TUMOR SUPPRESSOR gene (i).

Saccharin appears to cause cancerous changes in LIVER TISSUE within 8 weeks in animal studies. While the doses were >66% above the ADI levels (25mg/kg body weight vs. 15mg/kg), they are plausible for a person who consumes > 3 saccharin sweetened drinks in a day (i).

Chronic saccharin consumption in animal models increases creatinine significantly and may cause KIDNEY INJURY (iii).

Saccharin INCREASES URIC ACID, one of the key pathological mechanisms by which fructose metabolism HARMS our cardiometabolic health (iii).

Saccharin may cause changes in the microbiome that increase inflammation and disrupt METABOLIC FUNCTION (iv, v, vi).

Fasting Blood Glucose increased in an animal study after 7 weeks of saccharin supplementation.

However, a double-blind, parallel-arm RCT in humans failed to result in any significant microbiome and glucose tolerance changes. The study was relatively short (2 weeks) and the dose was equivalent to c. 2 saccharin sodas. While this dose equates to the ADI, it is possible that people consume more than 2 diet sodas per day, and that the longer term (>2 weeks) consequences may differ from this trial. More trials are needed.

(i) El-Sayed Alkafafy, M. et al. (2015) ‘Impact of aspartame and saccharin on the rat liver: Biochemical, molecular, and histological approach’, International Journal of Immunopathology and Pharmacology, 28(2), pp. 247-255

(ii) Amin, K.A. et al. (2016) ‘Effect of sweetener and flavoring agent on oxidative indices, liver and kidney function levels in rats’, Indian J Exp Biol. 54(1), pp. 56-63

(iii) Azeez, O.A. et al. (2019) ‘Long-Term Saccharin Consumption and Increased Risk of Obesity, Diabetes, Hepatic Dysfunction, and Renal Impairment in Rats’, Medicina, 55, p. 681

(iv) Labrecque, M.T. et al. (2015) ‘Impact of ethanol and saccharin on fecal microbiome in pregnant and non-pregnant mice’, J Pregnancy Child Health, 2,

(v) Bian, X. et al. (2017) ‘Saccharin induced liver inflammation in mice by altering the gut microbiota and its metabolic functions’, Food Chem Toxicol, 107, pp. 530-539

(vi) Suez, J. et al (2014) ‘Artificial sweeteners induce glucose intolerance by altering the gut microbiota’, Nature, 514(7521)(vii) S Leibowitz, A. et al (2018), ‘Saccharin Increases Fasting Blood Glucose but Not Liver Insulin Resistance in Comparison to a High Fructose-Fed Rat Model’, Nutrients. 2018 Mar 12;10(3):341/

(viii) Serrano J, et al (2021), ‘High-dose saccharin supplementation does not induce gut microbiota changes or glucose intolerance in healthy humans and mice’, Microbiome. 2021 Jan 12;9(1):11.

D-Tagatose (Tagatose)

Tagatose is a similar molecule to fructose and appears to have similar metabolic consequences. The question is how much is absorbed. Tagatose is promoted as a sugar that is not as readily absorbed and metabolized as sucrose. However, the amount absorbed and metabolized varies significantly in studies. In animal studies: the amount absorbed appears to be around 20% to 25%. Meanwhile, in human research, the absorbed and metabolized amount appears to range from 66% to 81% (i).

WHY AVOID?

If the amount absorbed and metabolized is discovered to be minimal in humans, then this sweet ingredient may be useful. However, until definitive research indicates this, tagatose has a similar metabolic pathway to fructose and is thus not helpful to consumers looking to reduce sugar consumption.

The tagatose that is metabolized ELEVATES URIC ACID levels, potentially to even greater degrees than fructose itself (ii). Elevated uric acid leads to pathology: it promotes fat gain, metabolic dysfunction, and cardiovascular disease risk.

Tagatose in animal research appears to induce significant increases in liver size, like that seen during high-sucrose and high-fructose diets (iii).

Further research is needed to confirm the % of tagatose that is absorbed and metabolized in humans at various doses, to uncover how much fuels a similar metabolic pathway to that of fructose.

(i) Normén, L. et al. (2001), ’Small-bowel absorption of d-tagatose and related effects on carbohydrate digestibility: an ileostomy study’, The American Journal of Clinical Nutrition, Volume 73, Issue 1, 2001,Pages 105-110, ISSN 0002-9165

(ii) Buemann, B. et al. (2000) ‘D-Tagatose, a stereoisomer of D-fructose, increases blood uric acid concentration’, Metabolism, 49(8)

(iii) Bär, A. et al. (1999) ‘Characteristics and significance of D-tagatose-induced liver enlargement in rats: An interpretative review’, Regul Toxicol Pharmacol. 29(2)

Sucralose

Sucralose is produced by chlorination of sugar and is a highly stable molecule, so much so that it is used to track water pollution. It is accumulating in the environment, with unknown long-term consequences. It was created during the production of an insecticide and is now used in many artificially-sweetened food and drink products.

WHY AVOID?

Sucralose appears to LOWER INSULIN SENSITIVITY - even at 15% of the ADI in healthy humans (ii) - and may cause HYPERINSULINEMIA and SIGNIFICANTLY INCREASED LIPOGENESIS (FAT CREATION) and inflammation (ii, iii).

Sucralose in healthy humans appears to lower insulin sensitivity in response to carbohydrates, and that this correlates to the brain’s sensitivity to sweet taste, even though the individuals’ sensory perception of sweetness remains (iv, v).

In vitro studies in stem cells indicate that sucralose may increase reactive oxygen species (ROS) and promote adipogenesis (vi).

Sucralose appears to increase ADIPOCYTE (FAT CELL) size significantly (via SREBP-1-induced hyperinsulinemia) and appears to cause whitening of adipocytes (FAT CELLS). Generally, it is a move away from metabolic health to have less brown adipose tissue (brown fat) and more white adipose tissue (iii).

Persistent (even low) sucralose consumption appears to lead to increased sweet taste receptors in the intestinal epithelium and GLUT2 (glucose transporter) in enterocytes, increasing glucose absorption in the gut and BLOOD GLUCOSE LEVELS. These phenomena are seen in obese subjects and are associated with INSULIN RESISTANCE, the very pathology that is meant to be averted by avoiding sugar (iii, vi, xi).

Sucralose appears to increase systemic INFLAMMATION via activating the toll-like-receptor (TLR)-4 signaling pathway (iii) and other inflammatory transcriptome pathways (viii).

Long-term sucralose consumption significantly results in WEIGHT GAIN, including visceral fat gain, HYPERINSULINEMIA and HYPERGLYCEMIA in animal models. Sucralose increased phosphorylation of cJun-N-terminal-kinase (JNK), which is associated with insulin resistance (x, iii). Similar results have been observed in normal-weight as well as obese humans. Even one sucralose dose caused elevated glycemic and insulin responses to an oral glucose test in obese individuals (ix).

Sucralose causes gut microbiome changes towards microbiome characteristics seen in humans with Type 2 diabetes, indicating that replacing sugar consumption with sucralose may lead to the same/similar pathology (i, vii, xii, xiii).

Sucralose may lead to INFLAMMATORY BOWEL DISEASE (IBD), exacerbate CROHN’S DISEASE and INTESTINAL PERMEABILITY (ix, xiv, xv, xvi).

Sucralose withstands heat, acidification, pH and temperature changes, and is NOT DEGRADED by WASTEWATER TREATMENT. It is ACCUMULATING in the ENVIRONMENT (it has been found in wastewater, rivers, estuaries and the Gulf Stream). It is contaminating micro-environments and we do not know the long-term consequences of this accumulating synthetic compound on environmental or human health (xvii).

Sucralose in the presence of glycerol generates toxic chloropropanols, as found in research on using sucralose in baked goods (xviii) – do not use sucralose for baking or cooking.

Women and children appear to be more vulnerable to the potentially negative effects of sucralose (xix, xx, xxi).

(i) Abou-Donia, M.B. et al. (2008) ‘Splenda alters gut microflora and increases intestinal p-glycoprotein and cytochrome p-450 in male rats’, J Toxicol Environ Health A., 71, pp. 1415-1429

(ii) Romo-Romo, A. et al. (2018) ‘Sucralose decreases insulin sensitivity in healthy subjects: a randomized controlled trial’, Am J Clin Nutr. (108), pp. 485–491

(iii) Sánchez-Tapia, M. et al. (2019) ‘Natural and Artificial Sweeteners and High Fat Diet Modify Differential Taste Receptors, Insulin, and TLR4-Mediated Inflammatory Pathways in Adipose Tissues of Rats’, Nutrients, 11(880)

(iv) Dalenberg, JR. et al (2020), ‘Short-Term Consumption of Sucralose with, but Not without, Carbohydrate Impairs Neural and Metabolic Sensitivity to Sugar in Humans’, Cell Metab. 2020 Mar 3;31(3):493-502.e7

(v) Gómez-Arauz, AY. (2019), ‘A Single 48 mg Sucralose Sip Unbalances Monocyte Subpopulations and Stimulates Insulin Secretion in Healthy Young Adults’, J Immunol Res. 2019 Apr 28; 2019:6105059.

(vi) Kundu, N. et al. (2020), ‘Sucralose promotes accumulation of reactive oxygen species (ROS) and adipogenesis in mesenchymal stromal cells’. Stem Cell Res Ther 11, 250 (2020).

(vii) Swithers, S.E. (2013) ‘Artificial sweeteners produce the counterintuitive effect of inducing metabolic derangements’, Trends in Endocrinology and Metabolism, 24(9).

(viii) Sylvetsky, AC. et al (2020), ‘Consumption of Diet Soda Sweetened with Sucralose and Acesulfame-Potassium Alters Inflammatory Transcriptome Pathways in Females with Overweight and Obesity’, Mol Nutr Food Res. 2020 Jun;64(11):e1901166.

(ix) Pepino, M.Y. et al. (2013) ‘Sucralose Affects Glycemic and Hormonal Responses to an Oral Glucose Load’, Diabetes Care, 36

(x) Ragi M-EE et al (2022), ‘The effect of aspartame and sucralose intake on body weight measures and blood metabolites: role of their form (solid and/or liquid) of ingestion. British Journal of Nutrition’, 2022;128(2):352-360.

(xi) Suez, J. et al. (2014) ‘Artificial sweeteners induce glucose intolerance by altering the gut microbiota’, Nature, 514(7521)

(xii) Dai, X. et al. (2020), ‘Maternal Sucralose Intake Alters Gut Microbiota of Offspring and Exacerbates Hepatic Steatosis in Adulthood’, Gut Microbes 2020, 11, 1043–1063.

(xiii) Bian, X. et al (2017), ‘Gut Microbiome Response to Sucralose and Its Potential Role in Inducing Liver Inflammation in Mice’, Front. Physiol. 2017, 8, 487.

(xiv) Qin, X. (2011) ‘What made Canada become a country with the highest incidence of inflammatory bowel disease: Could sucralose be the culprit?’, Can J Gastroenterol, 25(9)

(xv) Abou-Donia, M.B. et al. (2008) ‘Splenda alters gut microflora and increases intestinal p-glycoprotein and cytochrome p-450 in male rats’, J Toxicol Environ Health A., 71(21), pp. 1415-29

(xvi) Rodriguez-Palacios, A. et al. (2018) ’ The Artificial Sweetener Splenda Promotes Gut Proteobacteria, Dysbiosis, and Myeloperoxidase Reactivity in Crohn's Disease-Like Ileitis’, Inflamm Bowel Dis., 24(5), 1005-1020

(xvii) Omran, A. et al. (2013) ‘Metabolic Effects of Sucralose on Environmental Bacteria’, Journal of Toxicology, 2013

(xviii) Rahn, A. and Yaylayan, V.A. (2010) ‘Thermal degradation of sucralose and its potential in generating chloropropanols in the presence of glycerol’, Food Chemistry, 118, pp. 56-61

(xix) Yunker, A.G. et al. (2021), ‘Obesity and Sex-Related Associations With Differential Effects of Sucralose vs Sucrose on Appetite and Reward Processing: A Randomized Crossover Trial’, JAMA Netw Open. 2021;4(9):e2126313.

(xx) Sylvetsky, A.C. et al. (2017), ‘Plasma Concentrations of Sucralose in Children and Adults’, Toxicol. Environ. Chem. 2017, 99, 535–542

(xxi) Azad, MB. et al. (2020), ‘Nonnutritive sweetener consumption during pregnancy, adiposity, and adipocyte differentiation in offspring: evidence from humans, mice, and cells’, Int J Obes (Lond). 2020 Oct;44(10):2137-2148.

SUMMARY

NOMOSU avoids artificial sweeteners because:

1. Many have unpleasant tastes.

2. Evidence points to potentially undesirable biological effects.

3. There is an organic, delicious, health-promoting, sweet mix of natural ingredients that tastes great, makes you feel well while eating, and enhances gut health over time. Why use artificial sweeteners if they do not help with taste or health?

Explore The Full Collection

WHAT CAN YOU DO?

CHECK THE INGREDIENTS LABEL

Avoid or Minimize these Artificial Sweeteners:

Maltitol
Isomalt

Sorbitol
Acesulfame (Ace-K)

Aspartame and Neotame
Saccharin

Tagatose
Sucralose

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ARTIFICIAL SWEETENERS

Most Common ARTIFICIAL Sweeteners and WHY we AVOID them

Maltitol

WHY AVOID?

Isomalt

WHY AVOID?

Sorbitol

WHY AVOID?

Acesulfame K (Ace-K)

WHY AVOID?

Aspartame & Neotame

WHY AVOID?

Saccharin

WHY AVOID?

D-Tagatose (Tagatose)

WHY AVOID?

Sucralose

WHY AVOID?

SUMMARY

WHAT CAN YOU DO?

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