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Objective: To examine differences in the frequency and severity of federally reported adverse events between caffeine-containing and non-caffeine-containing products while also identifying the category of caffeine-containing products associated with the highest frequency and severity of adverse events., Patients and Methods: All adverse event reports that met specified eligibility criteria and were submitted to the Center for Food Safety and Applied Nutrition Adverse Event Reporting System between January 1, 2014, and June 29, 2018, were extracted. In this retrospective observational study, the most severe adverse event experienced, an ordinal variable, was categorized into death, life-threatening, hospitalization/disability, and emergency department visit. A nonproportional odds model was used to compare the odds of caffeine-containing products being associated with more severe adverse events relative to a noncaffeine group. The analysis is of data only from those reporting adverse events and may or may not be representative of the entire population exposed to these products, which is not known from the examined data., Results: Energy and preworkout products saw a significant increase in the odds of the adverse event experienced being death rather than the other less severe outcomes relative to the noncaffeinated group. Those products, along with weight loss products, had greater odds of the adverse event being death or life-threatening vs the less severe outcomes relative to the noncaffeinated group., Conclusion: Caffeine-containing products have a greater association with severe adverse events compared with non-caffeine-containing products. Exposure to preworkout and weight loss products had greater odds of being associated with a more serious adverse event relative to noncaffeinated products. Health care practitioners should use these outcomes to better inform and educate patients about the many factors related to caffeine intake and adverse outcomes., (Copyright © 2020 Mayo Foundation for Medical Education and Research. Published by Elsevier Inc. All rights reserved.)

Foodborne nanoparticles (NPs) have drawn great attention due to human health concerns. This study reports the detection of the presence of fluorescent NPs, about 5 nm, in two of the most popular beverages, Coca-Cola (Coke) and Pepsi-Cola (Pepsi). The NPs contain H, C and O, three elements with a tunable emission and with a quantum yield of 3.3 and 4.3% for Coke and Pepsi, respectively. The presence of sp 3 -hybridized carbon atoms of alcohols and ethers bonds was confirmed by NMR analysis. The NPs can be taken up by living cells and accumulate within cell membrane and cytoplasm. Evaluation of the acute toxicity of the NPs revealed that the BALB/c mice appeared healthy after administration of a single dose of 2 g kg -1 body weight. Analysis of glutamate pyruvate transaminase (GPT), glutamic oxaloacetic transaminase (GOT), urea and creatinine showed that there were statistically, but not biologically, significant differences in some of these biochemical parameters between the test and control groups. No obvious organ damage or apparent histopathological abnormality was observed in the tested mice. The biodistribution study in major organs indicated that the NPs were easily accumulated in the digestive tract, and they were able to cross the blood-brain barrier and dispersed in the brain. In vitro digestion of the NPs showed a significant fluorescence quenching of the NPs. This work represents the first report of foodborne fluorescent NPs present in Coke and Pepsi, and provides valuable insights into physicochemical properties of these NPs and their toxicity characteristics both in vitro and in vivo.

A significant association between fructose corn syrup in sweetened beverages consumption and increased risk of detrimental central nervous system effects has been recently reported. We hypothesized that the aspartame and soft drink induced disturbances in energy production and endocrine function, which play a role in the induction of brain damage. Therefore, we aimed to assess the effect of aspartame and soft drink on brain function and the link between energy status in the brain, oxidative stress and molecular pathways of apoptosis. Thirty rats were randomly assigned to drink water, aspartame (240 mg/kg orally) and cola soft drinks (free access) daily for two months. Subchronic intake of aspartame and soft drink significantly disrupted the brain energy production, as indicated by inhibited serum and brain creatine kinase, specifically in soft drink-received rats. Moreover, they substantially altered serum electrolytes (increased Ca and Na, and depleted Cu, Fe, Zn and K levels), and accordingly the related hormonal status (increased T4 and PTH, and lowered T3 and aldosterone levels), particularly in soft drink-received rats reflecting brain damage. Additionally, significant increment of acetylcholine esterase activity concomitant with the reduction of antioxidant molecules (SOD, CAT, GSH-Px and GSH), and induction of malondialdehyde level are precisely indicative of oxidative brain damage. Brain mRNA transcripts of target genes showed that aspartame and soft drink induced upregulation of BAX, Casp3, P27 and Mdm2 (1.5-fold) and down-regulation of Bcl2, suggesting an activation of cellular apoptosis. Collectively, subchronic aspartame and soft drink-induced brain damage in rats may be driven via a mechanism that involves energy production disruption, electrolytes and hormonal imbalance, increased oxidative stress and activation of molecular pathway of neuronal apoptosis.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common human enzyme defect often presenting with neonatal jaundice and/or hemolytic anemia. G6PD hemolytic events are linked with exposure to a pro-oxidant agent. We here report three cases of initial G6PD crises in breastfed children secondary to maternal consumption of a tonic drink which contains quinine. Quinine was found in breast milk of one of the mothers after she consumed tonic water., Conclusion: The amount of quinine that is transmitted through breast milk appears to be sufficient to induce G6PD crises in breastfed children. We hence recommend that consumption of quinine-containing sodas during breastfeeding should be avoided in populations with a high prevalence of G6PD deficiency. What is Known: • G6PD hemolytic events are linked with exposure to a pro-oxidant agent. • Ingestion of fava beans by a mother who was breastfeeding has been reported to induce a neonatal G6PD crisis. What is New: • Maternal consumption of tonic drink which contains quinine appears to be sufficient to induce G6PD crises in breastfed children. • Maternal consumption of quinine-containing sodas during breastfeeding should be avoided in populations with a high prevalence of G6PD deficiency.

In Saudi Arabia, the consumption of carbonated soft drinks is common and often occurs with each meal. Carbonated soft drink consumption has been shown to exhibit effects on the liver, kidney and bone. However, the effects of these soft drinks on brain activity have not been widely examined, particularly at the gene level. Therefore, the current study was conducted with the aim of evaluating the effects of chronic carbonated soft drink consumption on oxidative stress, brain gene biomarkers associated with aggression and brain histology. In total, 40 male Wistar rats were divided into four groups: Group 1 served as a control and was provided access to food and water ad libitum; and groups 2‑4 were given free access to food and carbonated soft drinks only (Cola for group 2, Pepsi for group 3 and 7‑UP for group 4). Animals were maintained on these diets for 3 consecutive months. Upon completion of the experimental period, animals were sacrificed and serological and histopathological analyses were performed on blood and tissues samples. Reverse transcription‑polymerase chain reaction was used to analyze alterations in gene expression levels. Results revealed that carbonated soft drinks increased the serum levels of malondialdehyde (MDA). Carbonated soft drinks were also observed to downregulate the expression of antioxidants glutathione reductase (GR), catalase and glutathione peroxidase (GPx) in the brain when compared with that in the control rats. Rats administered carbonated soft drinks also exhibited decreased monoamine oxidase A (MAO‑A) and acetylcholine esterase (AChE) serum and mRNA levels in the brain. In addition, soft drink consumption upregulated mRNA expression of dopamine D2 receptor (DD2R), while 5-hydroxytryptamine transporter (5‑HTT) expression was decreased. However, following histological examination, all rats had a normal brain structure. The results of this study demonstrated that that carbonated soft drinks induced oxidative stress and altered the expression of certain genes that are associated with the brain activity and thus should be consumed with caution.

Epidemiological studies have shown an association between the intake of cola beverages and chronic kidney diseases. Experimental evidence for the negative effects of cola intake on kidneys is lacking. Male Wistar rats had ad libitum access to water (control group) or three different sugar-sweetened cola beverages for three months. Despite very high cola intake (daily cca 140 mL), no differences were found in body weight, kidney weight, glomerular morphology, oxidative and carbonyl stress or expression of selected marker genes in the renal cortex. Interestingly, all groups consuming cola beverages had lower blood glucose levels during an oral glucose tolerance test, suggesting improved insulin sensitivity. Despite hyperfiltration (5-6-fold increase in diuresis), cola beverages had no effect on assessed parameters of renal function, histology, gene expression or oxidative stress. Moreover, cola intake seems to increase creatinine clearance and to decrease plasma levels of urea. In our study increased insulin sensitivity and altered renal functional parameters were observed in rats receiving cola beverages for three months. Whether the findings are due to the short duration of the study or interspecies metabolic differences should be uncovered in further studies. Even more interesting might be the analysis of effects of cola intake in animal models of diabetes.

Background: We examined the effect of sparkling water on gastroduodenal HCO3- secretion in rats and investigated the factors involved in these responses., Material/methods: Under urethane anesthesia, a chambered stomach or a proximal duodenal loop was superfused with saline, and HCO3- secretion was measured at pH 7.0 using a pH-stat., Results: The amount of CO2 in sparkling water was about 7.2 g/L. The mucosal exposure with sparkling water increased the secretion of HCO3- in both the stomach and duodenum. The HCO3- response in the duodenum was partially inhibited by indomethacin, acetazolamide or sensory deafferentation and was totally abolished by the co-administration of the former two agents. By contrast, the response in the stomach was almost totally inhibited by acetazolamide and partially mitigated by indomethacin but not sensory deafferentation. DIDS [an inhibitor of the Cl-/HCO3- exchanger (AE) and the Na+-HCO3- cotransporter (NBC)] and DMA [an inhibitor of the Na+/H+ exchanger 1 (NHE1)] partially mitigated the HCO3- response in the duodenum but not the stomach. The mucosal application of sparkling water increased prostaglandin E2 content in these tissues., Conclusions: Sparkling water stimulates HCO3- secretion in both the stomach and the duodenum, but the mechanisms involved differ in these two tissues; the response in the former is mainly due to the intracellular supply of HCO3- with the aid of carbonic anhydrase, while in the latter the response is dependent on the NHE1, AE and NBC, and is mediated by endogenous prostaglandins as well as capsaicin-sensitive afferent neurons, in addition to the intracellular supply of HCO3-.

Objectives: To evaluate the effects of a 6% hydrogen peroxide tooth whitener, Xtra White, on sound human enamel microhardness in vitro after an extended and exaggerated simulated 8 weeks of product use., Method and Materials: Polished human enamel specimens were prepared and baseline microhardness and color measurements determined. The enamel specimens were exposed to a fluoride-containing toothpaste for 30 seconds and then exposed to water, Xtra White, a control carbopol gel containing no hydrogen peroxide, or a carbonated beverage (each group, n = 8) for 20 minutes. Specimens were exposed to whole saliva at all other times. In order to simulate 8 weeks of extended product use, quadruple the length of the manufacturer's instructions, 112 treatments, were conducted. Microhardness measurements were taken after 2, 4, 6, and 8 weeks of simulated treatments, and color was measured after 2 and 8 weeks., Results: The Xtra White-treated specimens showed a statistically significant (P < .0001) increase in L* and decrease in b* compared to the water-treated specimens after 2 weeks simulated use, indicating bleaching had occurred. The carbonated beverage-treated specimens were significantly softened (P = .0009) compared to baseline after only 1 treatment. The carbopol gel-treated specimens were significantly softened (P = .0028) after 2 weeks of simulated treatments compared to baseline. There were no statistically significant differences in enamel microhardness between baseline and all treatment times for XW and water groups., Conclusion: Xtra White does not have any deleterious effects on sound human enamel microhardness after an extended and exaggerated simulated 8 weeks of product use.

Background: End-stage renal disease rates rose following widespread introduction of high fructose corn syrup in the American diet, supporting speculation that fructose harms the kidney. Sugar-sweetened soda is a primary source of fructose. We therefore hypothesized that sugary soda consumption was associated with albuminuria, a sensitive marker for kidney disease., Methodology/principal Findings: Design was a cross-sectional analysis. Data were drawn from the National Health and Nutrition Examination Survey (NHANES), 1999-2004. The setting was a representative United States population sample. Participants included adults 20 years and older with no history of diabetes mellitus (n = 12,601); after exclusions for missing outcome and covariate information (n = 3,243), the analysis dataset consisted of 9,358 subjects. Exposure was consumption of two or more sugary soft drinks, based on 24-hour dietary recall. The main outcome measure was Albuminuria, defined by albumin to creatinine ratio cutpoints of >17 mg/g (males) and >25 mg/g (females). Logistic regression adjusted for confounders (diet soda, age, race-ethnicity, gender, poverty). Interactions between age, race-ethnicity, gender, and overweight-obesity were explored. Further analysis adjusted for potential mediators: energy intake, basal metabolic rate, obesity, hypertension, lipids, serum uric acid, smoking, energy expenditure, and glycohemoglobin. Alternative soda intake definitions and cola consumption were employed., Results: Weighted albuminuria prevalence was 11%, and 17% consumed 2+ sugary soft drinks/day. The confounder-adjusted odds ratio for sugary soda was 1.40 (95% confidence interval: 1.13, 1.74). Associations were modified by gender (p = 0.008) and overweight-obesity (p = 0.014). Among women, the OR was 1.86 (95% CI: 1.37, 2.53); the OR among males was not significant. In the group with body mass under 25 kg/m(2), OR = 2.15 (95% confidence interval: 1.42, 3.25). Adjustment for potential mediators and use of alternative definitions of albuminuria and soda consumption did not appreciably change results. Diet sodas were not associated with albuminuria., Conclusions: Findings suggest that sugary soda consumption may be associated with kidney damage, although moderate consumption of 1 or fewer sodas does not appear to be harmful. Additional studies are needed to assess whether HFCS itself, overall excess intake of sugar, or unmeasured lifestyle and confounding factors are responsible.

Most soft drinks are acidic in nature and exposure to these drinks may result in enamel erosion. This study sought to measure the pH of 20 commercial brands of soft drinks, the dissolution of enamel resulting from immersion in these drinks, and the influence of pH on enamel loss. Comparison of the erosive potential of cola versus non-cola drinks as well as regular sugared and diet versions of the same brands was undertaken. The pH was measured immediately after opening the soft drink can. Enamel slices obtained from freshly extracted teeth were immersed in the soft drinks and weighed at baseline and after 6, 24, and 48 hours of immersion. Non-cola drinks had significantly higher pH values than cola drinks but showed higher mean percent weight loss. By contrast, sugared versions of the cola and non-cola drinks showed significantly lower pH values and higher mean percent weight loss than their diet counterparts. The pH value of the soft drink did not have a significant influence on the mean percent weight loss (r = -0.28). Prolonged exposure to soft drinks can lead to significant enamel loss. Non-cola drinks are more erosive than cola drinks. Sugared versions of cola and non-cola drinks proved to be more erosive than their diet counterparts. The erosive potential of the soft drinks was not related to their pH value.

1. Acute galactosamine (Gal) hepatitis was induced in rats drinking ad libitum either sodic bicarbonated water of Vichy Grande Grille (GG) or ordinary tap water (OH2). Two series of experiments were performed. 2. In the first series, Gal-induced hepatitis was moderate. Twenty four hours after IP Gal injection, GG treated rats had relative to OH2 treated rats a decrease of bile flow and BSP excretion, and an increase of serum transaminase and bilirubin. Seven days after Gal the liver had returned to normal except for an increase in biliary bilirubin and liver total lipids. 3. In the second series, Gal-induced hepatitis was severe. Twenty four hours after galactosamine administration, an increase in mortality after anesthesia was found in Gal/GG rats. An increase of liver size and total hepatic lipids was also observed, while bile secretion, BSP excretion, cyt P 450 and ARN decreased in Gal/GG rats. Steatosis and inflammatory reactions were more important in Gal/GG than in Gal/OH2 rats. Most parameters came back to their normal levels in two days in Gal/OH2 rats, while 7 days were generally necessary in Gal/GG treated animals. Hepatic DNA kept increasing in Gal/GG animals and was still higher after 7 days, maybe due to a greater inflammatory reaction in the liver, maybe following a stimulated hepatocyte regenerative response. 4. These results indicate that GG water is not an inoffensive salt solution.

Semiacute toxicity of cola fluid, Coca-Cola, conducting for approximately a month in rats, was studied. A trend of cariogenicity of Coca-Cola was strongly indicated. When the fluid was given ad libitum, decarbonized Coca-Cola and carbohydrate solution, consisted 8% of glucose and 3.5% of sugar and then adjusted pH to 2.4 with oxalic acid, were consumed 2 to 3 times greater than the control (water). A hyperuresis was observed as the result of great consumption of liquid, but no liver nor kidney degeneration was observed by histopathological examination. The diet consumption of the groups of Coca-Cola and carbohydrate solution was approximately a half of the control, water. However, when a complete diet was given, no physiological difference in time was observed, except in diarrhea and depression of hair gloss in Coca-Cola group.