Remember the basics? Serotonin and Norepinephrine control the appetite center of the brain. Aspartame metabolizes to phenylalanine, the AADC (Aromatic-L-amino acid decarboxylase) the enzyme metabolizes phenylalanine to PEA and synthesizes serotonin and dopamine.
Load aspartame, you load phenylalanine and knock out serotonin and dopamine synthesis.
The patient drinks diet pop thinking the zero calories will help a diet, meanwhile the neurotransmitters which suppress appetite are wiped out through AADC competitive inhibition. Increase hunger and weight gain ensues.
Bellow are a couple studies which verify that aspartame can cause weight gain.
Fueling the obesity epidemic? Artificially sweetened beverage use and long-term weight gain.
We have examined the relationship between artificially sweetened beverage (ASB) consumption and long-term weight gain in the San Antonio Heart Study. From 1979 to 1988, height, weight, and ASB consumption were measured among 5,158 adult residents of San Antonio, Texas. Seven to eight years later, 3,682 participants (74% of survivors) were re-examined. Outcome measures were incidence of overweight/obesity (OW/OB(inc)) and obesity (OB(inc)) (BMI > or = 25 and > or = 30 kg/m(2), respectively), and BMI change by follow-up (DeltaBMI, kg/m(2)). A significant positive dose-response relationship emerged between baseline ASB consumption and all outcome measures, adjusted for baseline BMI and demographic/behavioral characteristics. Consuming >21 ASBs/week (vs. none) was associated with almost-doubled risk of OW/OB (odds ratio (OR) = 1.93, P = 0.007) among 1,250 baseline normal-weight (NW) individuals, and doubled risk of obesity (OR = 2.03, P = 0.0005) among 2,571 individuals with baseline BMIs <30 kg/m(2). Compared with nonusers (+1.01 kg/m(2)), DeltaBMIs were significantly higher for ASB quartiles 2-4: +1.46 (P = 0.003), +1.50 (P = 0.002), and +1.78 kg/m(2) (P < 0.0001), respectively. Overall, adjusted DeltaBMIs were 47% greater among artificial sweetener (AS) users than nonusers (+1.48 kg/m(2) vs. +1.01 kg/m(2), respectively, P < 0.0001). In separate analyses--stratified by gender; ethnicity; baseline weight category, dieting, or diabetes status; or exercise-change category--DeltaBMIs were consistently greater among AS users. These differences, though not significant among exercise increasers, or those with baseline diabetes or BMI >30 kg/m(2) (P = 0.069), were significant in all 13 remaining strata. These findings raise the question whether AS use might be fueling--rather than fighting--our escalating obesity epidemic.
Department of Medicine, Division of Clinical Epidemiology, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA. email@example.com http://www.ncbi.nlm.nih.gov/pubmed/18535548
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