Aspartam och celldöd i hjärnan

[King Grub]

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.

Metab Brain Dis. 2017 Jun 28. Aspartame and Soft Drink-Mediated Neurotoxicity in Rats: Implication of Oxidative Stress, Apoptotic Signaling Pathways, Electrolytes and Hormonal Levels.

[King Grub]

Many controversial reports are available on the use of aspartame as it releases methanol as one of its metabolite during metabolism. The present study proposes to investigate whether long term (90 days) aspartame (40 mg/kg b.wt) administration could induce oxidative stress and alter the memory in Wistar strain male albino rats. To mimic the human methanol metabolism, methotrexate (MTX)-treated rats were included as a model to study the effects of aspartame. Wistar strain albino rats were administered with aspartame (40 mg/kg b.wt) orally and studied along with controls and MTX-treated controls. Aspartame interfered in the body weight and corticosterone levels in the rats. A marked increase in the mRNA and protein expression of neuronal nitric oxide synthase (nNOS) and induced nitric oxide synthase (iNOS) which resulted in the increased nitric oxide radical's level indicating that aspartame is a stressor. These reactive nitrogen species could be responsible for the altered cell membrane integrity and even cause death of neurons by necrosis or apoptosis. The animals showed a marked decrease in learning, spatial working and spatial recognition memory deficit in the Morris water maze and Y-maze performance task which could have resulted due to reduced hippocampal acetylcholine esterase (AChE) activity. The animal brain homogenate also revealed the decrease in the phosphorylation of NMDAR1-CaMKII-ERK/CREB signalling pathway, which well documents the inhibition of phosphorylation leads to the excitotoxicity of the neurons and memory decline. This effect may be due to methanol which may also activate the NOS levels, microglia and astrocytes, inducing neurodegeneration in brain. Neuronal shrinkage of hippocampal layer due to degeneration of pyramidal cells revealed the abnormal neuronal morphology of pyramidal cell layers in the aspartame treated animals. These findings demonstrate that aspartame metabolites could be a contributing factor for the development of oxidative stress in the brain.

J Food Drug Anal. 2018 Apr;26(2):903-916. Oxidative stress evoked damages leading to attenuated memory and inhibition of NMDAR-CaMKII-ERK/CREB signalling on consumption of aspartame in rat model.

[MaxTheMarketer]

Kroppen tillverkar ju naturliga antioxidanter. Har inte de till uppgift att motverka olika former av "oxidation" i kroppen, inklusive "oxidativ stress"? Är ej insatt i ämnet.

[Luca Brasi]

Aspartam är knappast den främsta källan till "aspartam-metaboliter" i blodet?

[King Grub]

The aim of the present study was to compare the effects of artificial sweeteners (aspartame, saccharin, and sucralose) on rat brain. Twenty-four adult male Sprague-Dawley rats were included in the study. The control group (n = 6) received regular tap water, whereas other groups received aspartame (3 mg/kg/day, n = 6,) or saccharin (3 mg/kg/day, n = 6) or sucralose (1.5 mg/kg/day, n = 6) in the drinking water. Following 6 weeks, the passive avoidance learning (PAL) test was performed to evaluate the neurobehavioral effects of sweeteners. The brains were assessed for lipid peroxides, neuron count, and Glial fibrillary acidic protein (GFAP) immunohistochemistry. Our results demonstrated that chronic intake of sweeteners significantly impaired PAL performance in all groups. Hippocampal CA1-CA3 areas revealed significantly lower neuronal count in aspartame and increased GFAP expression in all groups. Brain lipid peroxides were significantly higher in all groups. Our findings suggest that long-term consumption of artificial sweeteners may have harmful effects on cognition and hippocampal integrity in rats.

J Biochem Mol Toxicol. 2018 Apr 16:e22053. Evaluation of long-term effects of artificial sweeteners on rat brain: a biochemical, behavioral, and histological study.

[Luca Brasi]

Jättebra förklaringsmodell:

Att ständig utsättas för söt smak utan medföljande kaloriinnehåll fuckar upp diverse signalpeptider och sånt- mus hippocampusen krymper ihop på grund av att neurogenesen och skyddet mot neurotoxitet bryter ihop.

[King Grub]

Artificial sweeteners are mainly used as substitutes for sucrose derivates. In this study, we analyzed if the chronic consumption of aspartame or acesulfame potassium at an early age, produces histological alterations, astrogliosis and decreased neuronal viability, in hippocampus, prefrontal cortex, amygdala and hypothalamus of male Wistar rats. A histological analysis was performed on male Wistar rats that consumed aspartame or acesulfame potassium during 90 days, initiating the consumption of sweeteners immediately after weaning. The evaluation of neuronal morphology in different areas of the brain was performed with hematoxylin - eosin staining. To measure astrogliosis and neuronal viability, we used the immunohistochemical technique, with the glial fibrillary acidic protein immunomodulators (GFAP) and with neuronal-specific enolase (NSE). The consumption of aspartame or acesulfame potassium promoted morphological changes of neurons including increased pyknotic nuclei and vacuolization in all the brain areas studied. In hippocampus, prefrontal cortex, amygdala and hypothalamus, astrogliosis and reduction of neural viability were observed in sweeteners consumers in comparison with the control group. Chronic consumption of ASP and ACK from early stages of development and during long periods, may promote neural modifications, astrogliosis and decrease neuronal viability in prefrontal cortex, amygdala, hippocampus, and hypothalamus.

Metab Brain Dis. 2018 Sep 28. Astrogliosis and decreased neural viability as consequences of early consumption of aspartame and acesulfame potassium in male Wistar rats.

[Scratch89]

Men det smakar ju gött!

[Bob90]

Tur att man är "early age" då
Och att inta aspartam regelbundet i 90 dagar gör jag nog inte heller, tror jag.

[LunaSpice]

Ursprungligen postat av Bob90

Tur att man är "early age" då
Och att inta aspartam regelbundet i 90 dagar gör jag nog inte heller, tror jag.

Inte dagligt intag av smaksatt proteinpulver?

[Bob90]

Ursprungligen postat av LunaSpice

Inte dagligt intag av smaksatt proteinpulver?

Nope, blir max 0-3 ggr i veckan. Tror mitt mest frekventa och regelbundna intag är via tuggummi.

[LunaSpice]

Det här är väl en anledning att återgå till naturellt vasslepulver antar jag. *suck*

[Max]

Ursprungligen postat av Bob90

Tur att man är "early age" då
Och att inta aspartam regelbundet i 90 dagar gör jag nog inte heller, tror jag.

Observera att det är 90 rått-dagar. Om man över huvud taget skall försöka överföra resultatet så blir det många många dagar.

[Xtreme-G]

Ursprungligen postat av King Grub

Metab Brain Dis. 2018 Sep 28. Astrogliosis and decreased neural viability as consequences of early consumption of aspartame and acesulfame potassium in male Wistar rats.

Jag har kikat lite på studien. Råttorna fick aspartam i sitt vatten med koncentration 160 mg/ml. Aspartamsötad läsk får maximalt innehålla 0,6 mg/ml så det är ju inte jämförbart. Journalen verkar vara helt ok men artikeln har inte varit någon kioskvältare ännu med sina 13 nedladdningar på tre dagar.

Kanske inte bara är jag som blandat ihop enheterna?

In the present study the rodent’s daily consumption of ASP was approximately 54 mL of a solution of 160 mg/mL of ASP, which is equivalent to 62 mL of a 355 mL commercial light soda

[Xtreme-G]

Ursprungligen postat av Xtreme-G

Jag har kikat lite på studien. Råttorna fick aspartam i sitt vatten med koncentration 160 mg/ml. Aspartamsötad läsk får maximalt innehålla 0,6 mg/ml så det är ju inte jämförbart. Journalen verkar vara helt ok men artikeln har inte varit någon kioskvältare ännu med sina 13 nedladdningar på tre dagar.

Kanske inte bara är jag som blandat ihop enheterna?

Tog en extra titt och ser mitt misstag nu. De fick 160 mg/liter (inte per milliliter), vilket kan jämföras med läsk som får innehålla 600 mg/liter, alltså klart jämförbart med vanlig läsk. Endast 41 downloads och 4 shares av artikeln är dock ingen imponerande siffra, undra vad det beror på.