A Review on 132 Studies on Aspartame over 22 years
These studies suggest that aspartame, even at recommended safe dosages, might not be safe.
Several of these studies (in vitro as well as in vivo) that investigated both higher and safe dosages indicate that aspartame or its metabolites cause an oxidant/antioxidant imbalance, induce oxidative stress, and damage membrane integrity (lipid, protein, and nucleic acid), possibly affecting most cells and tissues. Aspartame is directly involved in the development of oxidative stress, which is a hallmark of systemic inflammation (Figure 3). Several animal studies have also reported a deleterious effect of aspartame exposure on body weight, adiposity, and/or glucose tolerance and insulin levels. These are summarized in a 2016 review by Fowler.125Thus, there is a need for additional detailed human studies and comprehensive characterizations of the physiological processes affected by aspartame. This is of particular importance, as diabetic and other individuals with gut dysbiosis may already be at increased risk of systemic inflammation because of the inflammatory nature of their conditions. Data reviewed in this paper suggest that aspartame use could not only exacerbate existing systemic inflammation but also cause inflammation if healthy individuals ingest it on a regular basis.
Blood Affected Affected Impaired delivery of oxygen to the tissues by red blood cells91,92; red blood cell aging91; altered neutrophil function93; decreased T-cell proliferation94; platelet hyperactivity and hyperaggregability95; upregulation of proinflammatory signaling96
Brain Affected Dysfunction of neuronal cells97; disruption of blood–brain barrier98; impaired neurobehavioral parameters (learning and memory)99; upregulation of neuroinflammation, which may initiate neurotropic effects100,101
Liver Affected Affected Loss of liver function102; inactivation of the heme group103,104; defect in synthesis of clotting factor105
Kidney Affected Affected Loss of kidney function106,107; weakening of acid–base balance106
Heart Affected Impaired cardiac function84; reduced heart rate variability75; and compensatory hypertrophy of myocytes85 caused by oxidative stress
Immune organs Affected Imbalanced oxidant/antioxidant status and variations in serum cytokine levels, eventually resulting in alteration of cellular and humoral immunity12,81,86,87
Gut microbes Affected Elevated fasting glucose and impaired insulin tolerance, mediated by alteration of the gut microbiota8
FDA APPROVED
Aspartame
Aspartame is approved for use in food as a nutritive sweetener. Aspartame brand names include Nutrasweet®, Equal®, and Sugar Twin®. It does contain calories, but because it is about 200 times sweeter than table sugar, consumers are likely to use much less of it.
FDA approved aspartame in 1981 (46 FR 38283) for uses, under certain conditions, as a tabletop sweetener, in chewing gum, cold breakfast cereals, and dry bases for certain foods (i.e., beverages, instant coffee and tea, gelatins, puddings, and fillings, and dairy products and toppings). In 1983 (48 FR 31376), FDA approved the use of aspartame in carbonated beverages and carbonated beverage syrup bases, and in 1996, FDA approved it for use as a “general purpose sweetener.” It is not heat stable and loses its sweetness when heated, so it typically isn’t used in baked goods.
Aspartame is one of the most exhaustively studied substances in the human food supply, with more than 100 studies supporting its safety. (Author: I was unable to find a single study proving that FDA suggested amounts are safe)
Conclusions: The results of this carcinogenicity bioassay confirm and reinforce the first experimental demonstration of APM’s multipotential carcinogenicity at a dose level close to the acceptable daily intake for humans. Furthermore, the study demonstrates that when life-span exposure to APM begins during fetal life, its carcinogenic effects are increased.
These studies have offered both support for, and biologically plausible mechanisms to explain, the results from a series of large-scale, long-term prospective observational studies conducted in humans, in which longitudinal increases in weight, abdominal adiposity, and incidence of overweight and obesity have been observed among study participants who reported using diet sodas and other LCS-sweetened beverages daily or more often at baseline. Furthermore, frequent use of diet beverages has been associated prospectively with increased long-term risk and/or hazard of a number of cardiometabolic conditions usually considered to be among the sequelae of obesity: hypertension, metabolic syndrome, diabetes, depression, kidney dysfunction, heart attack, stroke, and even cardiovascular and total mortality. Reverse causality does not appear to explain fully the increased risk observed across all of these studies, the majority of which have included key potential confounders as covariates. These have included body mass index or waist circumference at baseline; total caloric intake and specific macronutrient intake; physical activity; smoking; demographic and other relevant risk factors; and/or family history of disease. Whether non-LCS ingredients in diet beverages might have independently increased the weight gain and/or cardiometabolic risk observed among frequent consumers of LCS-sweetened beverages deserves further exploration. In the meantime, however, there is a striking congruence between results from animal research and a number of large-scale, long-term observational studies in humans, in finding significantly increased weight gain, adiposity, incidence of obesity, cardiometabolic risk, and even total mortality among individuals with chronic, daily exposure to low-calorie sweeteners – and these results are troubling
Awakening369 