‘Lone’ atrial fibrillation precipitated by monosodium glutamate and aspartame

Burkhart, Craig G.

doi:10.1016/j.ijcard.2009.01.028

Cited by 15 publications

(10 citation statements)

References 5 publications

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“…It has been also demonstrated that long-term vigorous exercise might contribute to the development of AF [25]. In addition, Burkhart CG reported that dietary elements such as monosodium glutamate and aspartame might have adverse effects on AF initiation [26,27]. However, the present study could not estimate the association between these factors and the incidence of AF.…”

Section: Discussionmentioning

confidence: 55%

Increased prevalence of atrial fibrillation after the Great East Japan Earthquake: Results from the Fukushima Health Management Survey

Suzuki

Ohira

Takeishi

et al. 2015

International Journal of Cardiology

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Section: Discussionmentioning

confidence: 55%

Increased prevalence of atrial fibrillation after the Great East Japan Earthquake: Results from the Fukushima Health Management Survey

Suzuki

Ohira

Takeishi

et al. 2015

International Journal of Cardiology

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“…However, the observations of the cardiac toxic effects of ASP are insufficient and only concern hypertension and electrocardiographic changes [ 10 ] or biochemical specifications [ 11 ]. Gudadhe et al [ 12 ] found that ASP caused hypertrophy of myocytes, due to an increase in the dimeter of the myocytes of mice.…”

Section: Introductionmentioning

confidence: 99%

Role of L-carnitine in protection against the cardiac oxidative stress induced by aspartame in Wistar albino rats

et al. 2018

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Aspartame (ASP) has been used as an alternative to sucrose for diabetics and obese people worldwide. Co-administration of L-carnitine (LC) with ASP has a protective effect against the liver and kidney toxicity induced of ASP. The goal of the investigation was to assess the enhancement of LC effect on the cardiac toxicity caused of ASP. The rats were divided into 6 groups: control with saline, LC (10 mg/kg), ASP (75 mg/kg), ASP (150 mg/kg), LC with 75 mg/kg of ASP, and LC with 150 mg/kg ASP. The antioxidants were determined by measuring the activities of myeloperoxidase, xanthine oxidase, superoxide dismutase, catalase, and glutathione peroxidase, and by assessing the levels of lipid peroxidation, total thiols, and glutathione. There was a significant elevation in LPO, in conjunction with a significant decline in the enzymatic antioxidants superoxide dismutase, catalase, and glutathione peroxidase and the non-enzymatic antioxidants glutathione and thiols. The cardiac myofibrils were found in a disarrayed pattern in ASP treated-animals as compared to the control rats. The animals treated with ASP-HD showed more than one apoptotic cell with a large tail and a small head, and the relaxed loops of the damaged DNA were extended to form a comet-shaped structure. These effects may be due to the excessive generation of reactive oxygen species by ASP, which reduces cardiac function. Co-administration of LC with ASP improved all of the above-mentioned parameters that were disrupted of ASP alone. This study evidences a sufficient originality in showing how LC plays a positive role against cardiac toxicity of ASP.

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“…Recently, Japan public healthcare heart study revealed that soft drink intake is related to incidence of ischemic heart disease and stroke [31]. In regarding association of aspartame and cardiovascular disease, aspartame can cause lone atrial fibrillation without hypertension [32]. These reports suggest that it has been strong positive association between aspartame consumption and incidence of myocardial infarction.…”

Section: Discussionmentioning

confidence: 99%

Modified High-Density Lipoproteins by Artificial Sweetener, Aspartame, and Saccharin, Showed Loss of Anti-atherosclerotic Activity and Toxicity in Zebrafish

et al. 2014

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Safety concerns have been raised regarding the association of chronic consumption of artificial sweeteners (ASs) with metabolic disorders, especially in the heart and brain. There has been no information on the in vivo physiological effects of AS consumption in lipoprotein metabolism. High-dosage treatment (final 25, 50, and 100 mM) with AS (aspartame, acesulfame K, and saccharin) to human high-density lipoprotein (HDL) induced loss of antioxidant ability along with elevated atherogenic effects. Aspartame-treated HDL3 (final 100 mM) almost all disappeared due to putative proteolytic degradation. Aspartame- and saccharin-treated HDL3 showed more enhanced cholesteryl ester transfer activity, while their antioxidant ability was disappeared. Microinjection of the modified HDL3 exacerbated the inflammatory death in zebrafish embryos in the presence of oxLDL. These results show that AS treatment impaired the beneficial functions of HDL, resulting in loss of antioxidant and anti-atherogenic activities. These results suggest that aspartame and saccharin could be toxic to the human circulation system as well as embryonic development via impairment of lipoprotein function.

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‘Lone’ atrial fibrillation precipitated by monosodium glutamate and aspartame

Cited by 15 publications

References 5 publications

Increased prevalence of atrial fibrillation after the Great East Japan Earthquake: Results from the Fukushima Health Management Survey

Increased prevalence of atrial fibrillation after the Great East Japan Earthquake: Results from the Fukushima Health Management Survey

Role of L-carnitine in protection against the cardiac oxidative stress induced by aspartame in Wistar albino rats

Modified High-Density Lipoproteins by Artificial Sweetener, Aspartame, and Saccharin, Showed Loss of Anti-atherosclerotic Activity and Toxicity in Zebrafish

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