If you have not read my previous articles about Aspartame you can
read each article by clicking on the links below.
The top 10 worst Sources of Aspartame
If you think you are making a healthier option because you chose to have diet soda over a regular soda drink, its time to think again. Crafty advertising may have given the term “sugar free” an impression of healthy alternative, but the truth of the matter is that chemical sweeteners are far from healthy.
Despite the dismissive stand of aspartame producers that aspartame is safe for human consumption, various studies over the years have shown that aspartame is actually linked to headaches, migraines, dizziness, tumors and even cancer. The U.S. FDA made public 92 symptoms attributed to aspartame from submitted complaints. Despite its questionable effect, aspartame was approved for use in 1981 and still continues to be so today. Ironically, aspartame was never tested in humans before its approval. Its use in over 6,000 products and by 250 million people has made the public its unwitting guinea pig in a grand experiment 40 years in the making.
Stocking up on diet foods is the best way to gain weight. Latest research on aspartame has revealed that it actually increases the risk of weight gain. Being 200 times sweeter than sugar, aspartame appears to be the perfect answer to dieting since it contains only a few calories while still having the sweet taste of sugar. Unfortunately, phenylalanine and aspartic acid, major components of aspartame, trigger the release of insulin and leptins. The latter are hormones that stimulate storage of body fat.
Moreover, large doses of phenylalanine lower serotonin levels and lead to food cravings. Since both real and artificial sweeteners stimulate the taste buds, they affect the same taste and pleasure pathways in the brain. Artificial sweeteners, however, merely activate but do not satiate the pleasure-related region of the brain, proving to be an inferior system in preventing sugar cravings. In the Yale Journal of Biology and Medicine, researcher Qing Yang – a faculty at the Department of Molecular, Cellular and Developmental Biology– published findings that revealed artificial sweeteners more likely to cause weight gain than weight loss.
This is over and above the fact that aspartame is also highly addictive. The phenylalanine and methanol components increase the dopamine levels in the brain and cause a certain high. This further creates an addiction that is only made worse by the release of methyl alcohol or methanol, which is considered a narcotic. Keeping this in mind, it’s time we reconsider the “health benefits” aspartame is supposed to give.
Products containing aspartame
The following are well-known products that use aspartame:
Diet Coca Cola (all varieties)Coca Cola Zero (all varieties)Diet Pepsi (all varieties)Pepsi Max (all varieties)Diet Irn Bru (all varieties)Lilt Zero (all varieties)Sprite Zero (all varieties)Tango (all varieties)Tango no added sugar (all varieties)7up Free (all varieties)Lucozade Sport (all varieties)Schweppes Slimline Drinks (all varieties)Fanta Zero (all varieties)Fanta OrangeDr Pepper ZeroOasis Summer Fruits Extra LightOasis Citrus Punch
Muller Light Cherry
Muller Light Blueberry
Muller Light Raspberry
Muller Light Banana and Custard
Danone Activia Cherry
Weight Watchers Fromage Frais
Weight Watchers Toffee and Vanilla
Wrigleys Airwaves (all varieties)
Wrigleys Orbit (all varieties)
Wrigleys Extra (all varieties)
Uncle Ben’s Sweet and Sour Light
Walkers Sensations Sweet Thai Chilli
Walkers Sensations Lime and Thai Spices
Walkers Prawn Cocktail
CanderelSilver Spoon Sweetness and LightSilver Spoon Light Granulated Sugar
Cadburys Highlights (all varieties)Options Hot Chocolate Drink (all varieties)
The above mentioned popular products are just a few of many that contain aspartame. Despite the rising reports of aspartame’s toxicity, a re-investigation by the FDA as well as of key regulatory bodies worldwide doesn’t seem to be coming anytime soon. We can only protect ourselves by making a conscious choice to check the label of every product we buy at the grocery store.
If you have complaints regarding aspartame, don’t be shy in making your complaint known. The last thing you want to be is a face in a crowd lining up before a government office that doesn’t have your interest at heart.
Our research demonstrated the lack of conclusive evidence as to the danger or safety of aspartame, and the necessity for more independent studies to ensure the health and wellbeing of consumers.
This topic is of significant interest because of the popularity of artificially-sweetened products within Western markets, and in particular the high consumption of aspartame in diet carbonated drinks within Australia. We chose this item as it had broad links to different areas studied within the course, including seizures, depression and pharmacological effects on the brain, but also because of its pertinence to our group: young women being the second highest consumers of aspartame-laden beverages (second only to sufferers of diabetes).
Aspartame is an white, odourless, powdered methyl ester comprised of aspartic acid and phenylalanine; hence its IUPAC name N-(L-?-Aspartyl)-L-phenylalanine,1-methyl ester (Figure 1). It is ~200 times sweeter than sucrose. While having a similar caloric profile to sucrose, its intensity of sweetness renders calorie intake negliable. It is slightly soluble in water (3×10-2 g mL-1 at ph 3 and 25oC). Solubility increases with high and low pH and heating, but various types of degredation also occur- in particularly strong acidic or alkaline conditions, aspartame may be used to produce methanol, or free amino acids via hydrolysis.
Aspartame was ‘discovered’ in 1965 when chemist James Schattler, while using aspartame in the development of an anti-ulcer drug, found it had a sweet flavour (ibid, p. 1806). At the time, Schattler was working for the G.D. Searle & Co. (now owned pharmaceutical giant Pfizer), who quickly patented it and put it up for approval for the consumable market by the Food and Drug Administration. While made legal in 1974, it was not until 1981 that Searle were permitted to market Aspartame in dry goods, and then in carbonated drinks in 1983 (GOA 1987, p. 2).
During the delay in marketing-approval, the FDA assessed the quality of Searle’s findings, as well as those of a 1975-1980 Public Board of Inquiry. While the PBI concluded that “aspartame did not cause brain damage… studies did not conclusively show that aspartame did not cause brain tumours” (ibid, p. 3). In the 1987 United States General Accounting Office’s review of Aspartame’s approval, scientists indicated “neurological function, brain tumours, seizures, headaches, and adverse effects on children and pregnant women” (ibid, p. 3) as being key areas which needed further investigation before approval could be given. While approval was given without addressing these concerns, research in all aforementioned issues continues.
After consumption, aspartame metabolises into two common amino acids, aspartic acid and phenylalanine, and methanol. While these can be harmful in large amounts, they are also naturally occurring in many of the foods we eat. In fact, foods such as milk, tomato juice and chicken have much higher amounts of these chemicals than aspartame. The chemical which has had the most focus from a neuroscientific perspective is phenylalanine, which is a Large Neutral Amino Acid (LNAA). Studies have focused on how consumption of it impacts upon the ratio of phenylalanine to other LNAAs, and whether this leads to inhibition of other important LNAAs and enzymes in the brain, such as decreased catecholamine, serotonin and dopamine concentrations. There are two fates for phenylalanine: firstly, some is metabolized in the liver to tyrosine, essential for the synthesis of important neurotransmitters such as dopamine (Figure 2a); secondly, phenylalanine readily crosses the blood brain barrier (BBB) by competing for binding on the NAAT, a co-transporter of phenylalanine, tryptopahn (precursor for serotonin) and other amino acids (Figure 2b and 2c). At high concentrations, the competitive binding of phenylalanine results in lower concentrations of dopamine hence disturbing its negative feedback pathway (Figure 2d). However, studies such as those by Stegink et al. (1996), show that while consumption of aspartame leads to a small increase in phenylalanine to LNAA ratio, it is not significant enough to cause any adverse effects. (Humphries, Pretorius & Naude, 2008)
High concentrations of phenylalanine will bind more effectively to NAAT, rather than tyrosine, hence leading to lower concentrations of dopamine. There are two pathways of uptake of phenylalanine in the body: (a) firstly, some phenylalanine is hydrolysed into tyrosine in the liver; and (b) secondly, phenylalanine will compete with tyrosine, methionine and other amino acids for binding on the NAAT and transported across the BBB. (c) Tyrosine must enter the BBB via NAAT since it cannot be synthesized in the brain. (d) Inside the brain, tyrosine is converted to dopamine. (Humphries, Pretorius & Naude, 2008, p. 453)
Aspartame also releases aspartate during digestion, a type of excitatory amino acid and neurotransmitter used by the neurons in the brain. Aspartate is purported to act on the NMDA receptors on the glutamate binding sites, causing calcium ion influx into the cell (Figure 3), thereby promoting greater chances of depolarization or increased firing of action potentials. This high rate of neuron depolarization can potentiate neurodegeneration (Humphries, Pretorius & Naude, 2008). Therefore, when such excitatory neurotransmitters are in excess, the potential toxicity may lead to the neuronal death in the CNS. Additionally, excess aspartame in extracellular space will pump back into glial cells by using enormous amounts of ATP; as the level of ATP stores decrease, the synthesis of glutamate and GABA also falls, thus affecting the functionality of glutamate. In essence, disrupting the balance of neurotransmitters potentially affects a wide range processes in the CNS and the rest of the body, such as amino acid metabolism.
It is purported that aspartate may act directly on the glutamate binding sites on the NMDA receptor, causing calcium ion influx and hence excitation. (“Neuroactive steroids: Synthesis of positive and negative modulators of NMDA receptor”, n.d.)
A headache is a common ailment in the general population due to pain caused by structures within the cranium (e.g. blood vessels, meninges), or structures outside the cranium (e.g. nerves, muscles). Aspartame has been accused of being a precipitant of headaches in consumer reports and questionnaires (Butchko et al., 2002). Yet, the unreliability of these studies have prompted further research using a double-blind crossover method. A double-blind crossover study conducted by Schiffman et al. (1987) did not find significance in the incidence of headaches in subjects who took aspartame compared to placebo. On the contrary, another study showed a subset of the study group were indeed more vulnerable to headaches (Van Den Eeden et al., 1994). However, this study only comprised a small sample of 33 subjects leading to potential statistical issues. Therefore, the answer to whether aspartame provokes headaches is still unclear given such variable reports.
Depression is a mood disorder characterized by many symptoms, including: depressed mood, loss of interest or pleasure, guilt, loss of appetite or overeating, and cognitive problems affecting concentration, memory or decision making. The ingestion of aspartame is suggested to increase the ratio of phenylalanine to other large neutral amino acids, possibly altering central neurotransmitter concentrations (Butchko et al., 2002). These alterations might modify brain function, such as mood or cognition. Walton, Hudak and Green-Waite (1993) conducted a study which examined the effect of aspartame on subjects already suffering from mood disorders; however, this study was cancelled due to severity of reactions in the initial 13 subjects. On the contrary, a completed study on healthy volunteers showed no significant effects of aspartame on mood or cognitive function (Spiers et al., 1998).
Phenylketonuria (PKU) is an autosomal recessive disease resulting in dysfunction in metabolism caused by deficiency of the enzyme, phenylalanine hydroxylase (PAH). PAH is essential for converting phenylalanine consumed in food to tyrosine, which is the precursor for dopamine, noradrenaline and adrenaline. As a consequence to deficient or inactive PAH, the concentration of phenylalanine in patients suffering from PKU can become toxic (“Pheylketonuria”, n.d.) since phenylalanine is hydrophobic, and competes with large, neutral amino acids to cross the blood brain barrier. Some common symptoms of PKU are neurological comprising of seizures, behavioural problems, psychiatric disorders and mental retardation. Therefore, aspartame consumption is theorized to cause adverse effects on vulnerable individuals, such as the heterozygous parents of PKU sufferers (PKUH). Despite this studies have once more produced inconclusive evidence, as some studies found high phenylalanine concentrations caused generalized EEG slowing (Epstein et al., 1989); whereas other data show no medical and biochemical changes (Koch, Shaw, Williamson, & Haber, 1976); nor significant effects on cognitive performance and EEGs (Trefz, et al., 1994). Further, a review by Butchko et al. (2002) on the vulnerability of PKUH to aspartame shows that several studies have demonstrated the tolerance of high levels of aspartame in PKUH, and studies employing more sophisticated EEG analysis found no statistically significant differences.
A brain tumour is an abnormal growth of cells within the brain or the central canal of the spinal cord, causing neurologic symptoms which are focal or generalised (DeAngelis, 2001). Generalized symptoms are due to intracranial hypertension leading to headaches, nausea and vomiting. Focal symptoms indicate the location of the tumour and can include weakness on one side of the body (hemiparesis) and impairment of producing or comprehending language (aphasia). One of the most controversial purported adverse effects of aspartame use is that it causes brain tumours. Investigations conducted in the 1970s showed a high occurrence of brain tumours in rats exposed to aspartame (Reynolds, Butler & Lemkey-Johnston, 1976). A more recent rat study showed a statistically significant increase in malignant schwannomas (cancer of Schwann cells on peripheral nerves), in addition to other cancers (Soffritti et al., 2006). Thus, suggesting that aspartame is a potential carcinogenic agent, particularly affecting the central nervous system.
Consequently, there is much controversy regarding whether aspartame may be a causative factor in human brain tumours. The incidence of human brain tumours increased significantly in the United States within 1-2 years following the approval of aspartame by the FDA (Roberts, 1991). A comparison of total CNS tumour trends showed a substantial fluctuation pre- and post-aspartame introduction in the US (Olney, Farber, Spitznagel & Robins, 1996). Given results from rat studies and the correlation between aspartame approval and brain tumour incidences, it is highly suggestive that aspartame causes brain tumours.
However, the same experimental procedure which found hypothalamic lesions in neonatal mice had no effect on infant monkeys (Reynolds, Butler & Lemkey-Johnston, 1976), indicating that primates may manage high amino acid loads better than rats, metabolically or at the level of the blood brain barrier. Furthermore, recent research found no risk associated with aspartame and brain cancer (Lim et al., 2006).
A seizure generally manifests in physical convulsions or other physical signs and the underlying mechanism is due to uncontrolled electrical activity in the brain. Given that aspartame is a purported excitotoxin, consumption may cause disturbance to the balance of central neurotransmitters, hence provoking seizures. In animal models aspartame promoted an increase in seizure frequency in those that were already at risk, yet it is unclear whether these results translate to humans (Maher & Wurtman, 1987). Although self reports of aspartame induced seizures may appear to be significant, a double-blind crossover model applied to such indivudals did not cause seizures even though phenylalanine concentrations were found to be significantly higher with aspartame consumption (Spiers et al, 1998).
A study by Helali et. al (1996) suggested that aspartame played an antagonistic role against anti-epileptic drugs possibly through decreased epinephrine and norepinephrine levels and increased GABA levels. Some studies (i.e. Sze, 1989) have shown that doses of 1000 mg aspartame/kg body weight (bw) or greater did enhance chemically induced seizures, however according to the review by Magnusson et. al. (2007), these results were not consistent, as another study (Reynolds et. al., 1984) claimed that doses of 2000 mg/kg bw had no effect on inducing seizures. There has been a general consensus amongst nearly all studies that doses of under 1000 mg/kg bw have no effect on inducing seizures. Considering that the average amount of aspartame consumed by the top-consuming 90th percentile of society is around 2-3 mg/kg bw, there should be very little concern for seizures as a symptom of aspartame consumption.
As becomes clearly apparent from our research, there is no conclusive evidence to suggest that aspartame is dangerous or safe for consumption. It would be our recommendation that more studies with improved methodologies commence so as to ensure the safety of the public.