Is Aspartame Just Pro-diabetic, Or So Much More?
A plethora of synthetic sweeteners are now available as an alternative to cane sugar and high-fructose corn syrup. Aspartame is one of the most prevalent, promoted for its supposed benefits to the obese and diabetic alike in a myriad of diet or low-calorie beverages and foods, and yet it is linked to disturbing research indicating that it may in fact be worse than the sugars it replaces.
The history of aspartame is a fascinating story for the student of political intrigue who is interested in the way that the vested interests of the food industry operate. Tactics have involved extensive lobbying, misinformation campaigns, pseudo-science and a controversial approval by the American Food And Drug Administration (FDA), which went against the findings of its own scientists concerning the dangers of this novel chemical. The FDA initially banned aspartame as a food additive due to concerns about its link with brain tumours, an obstacle created by the Delaney Amendment in 1958, which states carcinogens cannot be used as food additives; however, the manufacturer was able to influence the incoming US president during the year 1981 and, as a result, aspartame was more favourably appraised by the internal scientific committee assessing its toxicity.
Aspartame is usually indicated on food labels as an additive bearing the European code E951, yet it often appears in combination with other synthetic sweeteners such as saccharine and acesulfame-k, which improve the resemblance in taste to natural sucrose. Aspartame was first approved for dry foods in 1981, then carbonated drinks in 1983, and for general purposes in 1996. For instance, over 4500 tons have been used in the manufacture of beverages alone in 2006, or about 86% of production.2 It is an ingredient in hundreds of thousands of products such as sweetened beverages, confectionary, cereals, yoghurt, vitamins, cough drops and other pharmaceutical drugs so that it is consumed by some 200 million people worldwide.1
Aspartame and other synthetic sweeteners are commonly preferred by dieters who want to avoid energy-rich carbohydrates. Despite this advantage, these sweeteners are not stable on the shelf and present the problem of toxicity arising from the break-down metabolites produced in the product before consumption. In the case of aspartame these are aspartic acid, phenylalanine and methanol.
Aspartic acid is a common amino acid which acts as a neurotransmitter by stimulation N-methyl-D-aspartate receptor (NMDA) receptors on nerve cells, so when consumed in quantity it is theoretically a ‘excitotoxin’. The stimulating effect will also be magnified by caffeine or guarana, although by different mechanisms. The metabolite methanol is broken down into the toxic compounds formic acid, formaldehyde and the diketopiperazine (DKP), a process which requires robust liver detoxification, good nutrient status and optimal antioxidant defences, all of which are not generally found in people subsisting on ultra-processed foods under normal urban conditions. Unfortunately, in the absence of these efficient defences the mitochondria of cells are damaged, degenerative disease processes get underway, and aging is accelerated.
The combination of various sweeteners presents the added problem of their synergy with each other, as well as other industrial food additives, and some telling research has been done with mice on the subject of neurotoxicity. For example, the common food additives Brilliant Blue, L-glutamic acid and Quinoline Yellow were tested in combination with aspartame in one experiment, and the researchers found that these chemicals could have an additive effect on the cell toxicity arising from synthetic sweeteners.3
The synergy of aspartame with another common food additive, monosodium glutamate (MSG), which also adversely stimulates the NMDA receptor, was tested in another interesting laboratory experiment. This test proved that aspartame had an additive effect in the promotion of hyperglycaemia and insulin resistance, an astounding result given that low-calorie sweeteners are marketed as ‘healthy’ alternatives for people with diabetes.4
The above-mentioned scientific paper was limited to studying the effects of aspartame on rodents, but it quoted other research on the ‘zebra fish nutritional model’; nevertheless, the comparison can only go so far with primates in the real urban world of shopping malls can’t it? Well, there is actually quite a bit of research on humans too: to begin with, a link between the consumption of ‘diet’ beverages and metabolic syndrome has been well-established in several studies, but the mechanism is difficult to understand due to the fact that these beverages contribute little energy or other nutrients.
Before examining research into the actual mechanisms of blood sugar disruption, an interesting association has also been found in epidemiological studies. In one piece of research, called the Multi-Ethnic Study Of Atherosclerosis (MESA), the dietary habits of almost 7000 Caucasian, African, American, Hispanic, and Chinese adults were studied over a period of seven years. Blood lipids and blood sugar were measured, and various lifestyle confounders were taken into account. The result was that both incident metabolic syndrome and type 2 diabetes were associated with ‘diet soda’ consumption, as well as a higher waist circumference and fasting blood sugar. The authors concluded that these results ‘corroborate findings from the Atherosclerosis Risk in Communities and Framingham studies.’5
Part of the explanation for the disruptive effect may lie in the fact that synthetic sweeteners like aspartame pass into the intestines and interact directly with the gut microbes (the microbiome), or what we used to call ‘gut flora’. It is known that diet can cause rapid changes to the gut flora in humans, which in turn exerts powerful effects on physiology and metabolism, a condition known as dysbiosis when it produces adverse health effects. This is especially the case for a diet high in red meat and processed foods which contains a lot of sugar and fat, compared to a largely plant-based diet abundant in fibre and phytonutrients.6
In one experiment, three groups of mice fed saccharin, sucralose or aspartame for 11 weeks, soon developed glucose intolerance, when compared to a control group fed just glucose or sucrose. Saccharin showed the most pronounced effect, ‘displaying considerable dysbiosis’. The changes to the microbiota included ‘over-representation of Bacteroides and under-representation of Clostridiales’, of the type noted in type 2 diabetes in humans.7
Not only do so-called ‘diet’ soft drinks lead to a higher waist circumference and other general markers of metabolic syndrome, like dysbiosis, but they also promote local and systemic oxidative stress, a more insidious problem associated with chronic inflammation and organ damage. There is even good evidence of mitochondrial toxicity leading to cell death.8
An initial sign that that the body is under increased metabolic stress is a raised cortisol level. We find this with regular aspartame consumption, followed by altered blood sugar and insulin resistance.9 The finding that rats ingesting aspartame have correspondingly lower levels of the important cellular antioxidant glutathione in the brain, is proof of the depletion of these crucial defences, and should interest anyone who is concerned about getting early-onset dementia.10
It could be said that this heightened dementia risk is added to more specific disorders to do with brain function such as headaches, insomnia, and seizures. The development of specific mental disorders is also under review due to widespread effects on brain function: ‘aspartame disturbs amino acid metabolism protein structure and metabolism, integrity of nucleic acids, neuronal function, endocrine balances and changes in the brain concentration of catecholamines.’11
Sexual health is another matter, and aspartame is of particular concern to men. In an alarming experiment endured by a group of male rats, receiving ‘oral intubations of FDA approved aspartame’ over 90 days, the results indicated that sperm function was significantly decreased along with the number of cells which secrete testosterone. The damage, apparently caused by oxidative stress, was attributed to the toxic metabolite methanol.12
Any evidence concerning problems with blood sugar or blood lipids should also alert us to the possibility of heart disease when associated with the consumption of ‘light’ diet products. In this respect, one important finding is that synthetic sweeteners such as aspartame, saccharin, and acesulfame-k cause damage to plasma proteins such apoA-1 in a dose-dependent manner. This occurs via a similar pathway to the Maillard reaction, where toxic advanced glycation end products (AGEs) are produced. Importantly, this occurs in low concentrations, especially with saccharin and acesulfame-k, contributing to ‘severe premature cellular senescence and atherosclerosis.’13
Perhaps the most frightening of the pathologies that are possible when homeostasis is chronically disturbed, is cancer. In fact carcinogenesis caught the attention of toxicologists at the FDA at the pre-approval stage of aspartame, a long time ago, during bioassays in the 1970s on rodents. These were conducted by the same firm which manufactured aspartame, G.D. Searle. In these studies, rats were fed aspartame in various amounts for 104 weeks, which is about 2/3 of their lifespan, or roughly equivalent to humans at 60-65 years of age. The design of these experiments, which produced data that was not definitive in labelling aspartame a carcinogen, has been much criticised when assessed by today’s standards, which include pointing out the obvious conflict of interest; however, they still show some important trends in carcinogenesis especially amongst female rats, where an increase in malignant tumours was evident compared to controls in two of the experiments.14
Not surprisingly, later independent research on rodents by the Cesare Maltoni Cancer Research Center conclusively demonstrated aspartame to be a ‘multipotential carcinogenic agent’ (malignant tumours, lymphoma, leukaemia, kidney carcinoma, cancer of the ureter, nervous system schwannomas). This occurred at various daily doses as low as 20mg/kg which is equivalent to recommended daily intake for humans.1
This research was sternly rebutted by the food industry; meanwhile, concerned scientists have been steadily contributing to the evidence that demonstrates aspartame is much more than just a pro-diabetic agent. In fact, regular aspartame consumption helps prepare the general background conditions (terrain) necessary for just about any kind of degenerative disease to develop in the body, even at recommended safe levels. In one significant review of the literature, the researchers concluded that aspartame may ‘disrupt the oxidant/antioxidant balance, induce oxidative stress, and damage cell membrane integrity, potentially affecting a variety of cells and tissues and causing a deregulation of cellular function, ultimately leading to systemic inflammation.’15
This article is an extract from the eBook Sweet Tooth, Rotten Health.
References:
1. Belpoggi F, Soffritti M, Padovani M, Degli Esposti D, Lauriola M, Minardi F. Results of long-term carcinogenicity bioassay on Sprague-Dawley rats exposed to aspartame administered in feed. Ann N Y Acad Sci 2006;1076:559–77.
2. Schernhammer ES, Bertrand KA, Birmann BM, Sampson L, Willett WC, Feskanich D. Consumption of artificial sweetener- and sugar-containing soda and risk of lymphoma and leukemia in men and women. Am J Clin Nutr 2012;96:1419–28.
3. Lau K, McLean WG, Williams DP, Howard CV. Synergistic interactions between commonly used food additives in a developmental neurotoxicity test. Toxicol Sci Off J Soc Toxicol 2006;90:178–87.
4. Collison KS, Makhoul NJ, Zaidi MZ, et al. Interactive effects of neonatal exposure to monosodium glutamate and aspartame on glucose homeostasis. Nutr Metab 2012;9:58.
5. Nettleton JA, Lutsey PL, Wang Y, Lima JA, Michos ED, Jacobs DR. Diet soda intake and risk of incident metabolic syndrome and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA). Diabetes Care 2009;32:688–94.
6. David LA, Maurice CF, Carmody RN, et al. Diet rapidly and reproducibly alters the human gut microbiome. Nature 2014;505:559–63.
7. Suez J, Korem T, Zeevi D, et al. Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature 2014;514:181–6.
8. Horio Y, Sun Y, Liu C, Saito T, Kurasaki M. Aspartame-induced apoptosis in PC12 cells. Environ Toxicol Pharmacol 2014;37:158–65.
9. Choudhary AK. Aspartame: should individuals with Type II Diabetes be taking it? Curr Diabetes Rev 2017;
10. Abhilash M, Sauganth Paul MV, Varghese MV, Nair RH. Long-term consumption of aspartame and brain antioxidant defense status. Drug Chem Toxicol 2013;36:135–40.
11. Humphries P, Pretorius E, Naudé H. Direct and indirect cellular effects of aspartame on the brain. Eur J Clin Nutr 2008;62:451–62.
12. Ashok I, Poornima PS, Wankhar D, Ravindran R, Sheeladevi R. Oxidative stress evoked damages on rat sperm and attenuated antioxidant status on consumption of aspartame. Int J Impot Res 2017;29:164–70.
13. Jang W, Jeoung NH, Cho K-H. Modified Apolipoprotein (apo) A-I by Artificial Sweetener Causes Severe Premature Cellular Senescence and Atherosclerosis with Impairment of Functional and Structural Properties of apoA-I in Lipid-Free and Lipid-Bound State. Mol Cells 2011;31:461–70.
14. Soffritti M, Padovani M, Tibaldi E, Falcioni L, Manservisi F, Belpoggi F. The carcinogenic effects of aspartame: The urgent need for regulatory re-evaluation. Am J Ind Med 2014;57:383–97.
15. Choudhary AK, Pretorius E. Revisiting the safety of aspartame. Nutr Rev 2017;75:718–30.