Artificial sweeteners (aspartame bv) hebben een negatief effect op je Verzadiging (Video) Harvard Un

[houston]

http://www.amazon.com/When-Your-Child-Has-Disability/dp/1557664722/

Laat je moeder deze aanschaffen.

Klik om te verkleinen...

Randdebiel en mij staatsmongool noemen gaat erg ver en nu zelfs met deze link ben je zeer gevaarlijk bezig.
Zit jij ook al aan de steroiden en drugs (lafaard) zet even je echt naam op het forum en wat foto's!


Ik zal klachten indienen bij de mods.


Calyptus heeft toch wel iets een hoger niveau. Maarja jij bent natuurlijk ook maar een computer nerd op de universiteit van Amsterdam.

 

[Calyptus]

Randdebiel en mij staatsmongool noemen gaat erg ver en nu zelfs met deze link ben je zeer gevaarlijk bezig.
Zit jij ook al aan de steroiden en drugs (lafaard) zet even je echt naam op het forum en wat foto's!


Ik zal klachten indienen bij de mods.

Klik om te verkleinen...

http://www.youtube.com/watch?v=mwCZjGO6HIA

 

[houston]

http://www.amazon.com/When-Your-Child-Has-Disability/dp/1557664722/

Laat je moeder deze aanschaffen.

Klik om te verkleinen...

Misschien herken jij je zelf hierin!

http://www.ergogenics.org/kwart-chemische-bodybuilders-gebruikt-ook-groeihormoon.html

 

[Robjee]

Randdebiel en staatsmongool zijn bewoordingen die hier niet thuishoren, maar dat terzijde.

De gelinkte video heeft wetenschappelijk gezien geen waarde. Het draait om resultaten uit onderzoek en om deze in een juiste conext te plaatsen. Dus niet selectief één onderzoek eruit lichten. Richard Mattes et al. schrijven in een review:

Thus, short-term trials of NNS consumption provide mixed evidence supporting reduced energy intake, whereas longer-term trials consistently indicate that the use of NNS results in incomplete compensation and slightly lower energy intakes. The latter studies are arguably the more nutritionally relevant. These conclusions are consistent with those of previous reviewers ( 9, 23, 24, 26– 29, 45, 63).
http://ajcn.nutrition.org/content/89/1/1.full.pdf

@Houston, heb je ook bronnen naar wetenschappelijke literatuur?

 

[Galen]

Randdebiel en mij staatsmongool noemen gaat erg ver en nu zelfs met deze link ben je zeer gevaarlijk bezig.
Zit jij ook al aan de steroiden en drugs (lafaard) zet even je echt naam op het forum en wat foto's!


Ik zal klachten indienen bij de mods.


Calyptus heeft toch wel iets een hoger niveau. Maarja jij bent natuurlijk ook maar een computer nerd op de universiteit van Amsterdam.

Klik om te verkleinen...

Zo ver gaat het niet hoor, merely stating the obvious.

 

[houston]

Randdebiel en staatsmongool zijn bewoordingen die hier niet thuishoren, maar dat terzijde.

De gelinkte video heeft wetenschappelijk gezien geen waarde. Het draait om resultaten uit onderzoek en om deze in een juiste conext te plaatsen. Dus niet selectief één onderzoek eruit lichten. Richard Mattes et al. schrijven in een review:

Thus, short-term trials of NNS consumption provide mixed evidence supporting reduced energy intake, whereas longer-term trials consistently indicate that the use of NNS results in incomplete compensation and slightly lower energy intakes. The latter studies are arguably the more nutritionally relevant. These conclusions are consistent with those of previous reviewers ( 9, 23, 24, 26– 29, 45, 63).
http://ajcn.nutrition.org/content/89/1/1.full.pdf

@Houston, heb je ook bronnen naar wetenschappelijke literatuur?

Klik om te verkleinen...

http://www.ncbi.nlm.nih.gov/pubmed/12782208

Physiol Behav. 2003 Apr;78(4-5):557-62.
Physiological mechanisms mediating aspartame-induced satiety.
Hall WL, Millward DJ, Rogers PJ, Morgan LM.
Source

Centre for Nutrition and Food Safety, School of Biomedical and Life Sciences, University of Surrey, Guildford, Surrey GU2 7XH, UK. w.l.hall@reading.ac.uk
Abstract

Aspartame has been previously shown to increase satiety. This study aimed to investigate a possible role for the satiety hormones cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) in this effect. The effects of the constituents of aspartame, phenylalanine and aspartic acid, were also examined. Six subjects consumed an encapsulated preload consisting of either 400 mg aspartame, 176 mg aspartic acid+224 mg phenylalanine, or 400 mg corn flour (control), with 1.5 g paracetamol dissolved in 450 ml water to measure gastric emptying. A 1983-kJ liquid meal was consumed 60 min later. Plasma CCK, GLP-1, glucose-dependent insulinotropic polypeptide (GIP), glucose, and insulin were measured over 0-120 min. Gastric emptying was measured from 0 to 60 min. Plasma GLP-1 concentrations decreased following the liquid meal (60-120 min) after both the aspartame and amino acids preloads (control, 2096.9 pmol/l min; aspartame, 536.6 pmol/l min; amino acids, 861.8 pmol/l min; incremental area under the curve [AUC] 60-120 min, P<.05). Desire to eat was reduced from 60 to 120 min following the amino acids preload (control, -337.1 mm min; aspartame, -505.4 mm min; amino acids, -1497.1 mm min; incremental AUC 60-120 min, P<.05). However, gastric emptying rates, plasma CCK, GIP, insulin, and glucose concentrations were unaffected. There was a correlation between the increase in plasma phenylalanine and decrease in desire to eat after the liquid meal following the constituent amino acids (r=-.9774, P=.004). In conclusion, it is unlikely that aspartame increases satiety via CCK- or GLP-1-mediated mechanisms, but small changes in circulating phenylalanine concentrations may influence appetite.

 

[Galen]

http://www.ncbi.nlm.nih.gov/pubmed/12782208

Physiol Behav. 2003 Apr;78(4-5):557-62.
Physiological mechanisms mediating aspartame-induced satiety.
Hall WL, Millward DJ, Rogers PJ, Morgan LM.
Source

Centre for Nutrition and Food Safety, School of Biomedical and Life Sciences, University of Surrey, Guildford, Surrey GU2 7XH, UK. w.l.hall@reading.ac.uk
Abstract

Aspartame has been previously shown to increase satiety. This study aimed to investigate a possible role for the satiety hormones cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) in this effect. The effects of the constituents of aspartame, phenylalanine and aspartic acid, were also examined. Six subjects consumed an encapsulated preload consisting of either 400 mg aspartame, 176 mg aspartic acid+224 mg phenylalanine, or 400 mg corn flour (control), with 1.5 g paracetamol dissolved in 450 ml water to measure gastric emptying. A 1983-kJ liquid meal was consumed 60 min later. Plasma CCK, GLP-1, glucose-dependent insulinotropic polypeptide (GIP), glucose, and insulin were measured over 0-120 min. Gastric emptying was measured from 0 to 60 min. Plasma GLP-1 concentrations decreased following the liquid meal (60-120 min) after both the aspartame and amino acids preloads (control, 2096.9 pmol/l min; aspartame, 536.6 pmol/l min; amino acids, 861.8 pmol/l min; incremental area under the curve [AUC] 60-120 min, P<.05). Desire to eat was reduced from 60 to 120 min following the amino acids preload (control, -337.1 mm min; aspartame, -505.4 mm min; amino acids, -1497.1 mm min; incremental AUC 60-120 min, P<.05). However, gastric emptying rates, plasma CCK, GIP, insulin, and glucose concentrations were unaffected. There was a correlation between the increase in plasma phenylalanine and decrease in desire to eat after the liquid meal following the constituent amino acids (r=-.9774, P=.004). In conclusion, it is unlikely that aspartame increases satiety via CCK- or GLP-1-mediated mechanisms, but small changes in circulating phenylalanine concentrations may influence appetite.

Klik om te verkleinen...

En wat voor influence zou dat zijn afleidend uit de rest van het abstract... ?

Tevens:

Veel oude onderzoeken op Pubmed omtrent dit verhaal. Dit is door Harvard goed onderzocht. 1 van de weinige universiteiten die niet met de industrie werkt en nauwelijks frauderende wetenschappers in dienst heeft.

Klik om te verkleinen...

Is hierop van toepassing, dus waarom haal je hem aan

 

[houston]

http://www.ncbi.nlm.nih.gov/pubmed/19056571

Am J Clin Nutr. 2009 Jan;89(1):1-14. doi: 10.3945/ajcn.2008.26792. Epub 2008 Dec 3.
Nonnutritive sweetener consumption in humans: effects on appetite and food intake and their putative mechanisms.
Mattes RD, Popkin BM.
Source

Department of Foods and Nutrition, Purdue University, West Lafayette, IN, USA.
Abstract

Nonnutritive sweeteners (NNS) are ecologically novel chemosensory signaling compounds that influence ingestive processes and behavior. Only about 15% of the US population aged >2 y ingest NNS, but the incidence is increasing. These sweeteners have the potential to moderate sugar and energy intakes while maintaining diet palatability, but their use has increased in concert with BMI in the population. This association may be coincidental or causal, and either mode of directionality is plausible. A critical review of the literature suggests that the addition of NNS to non-energy-yielding products may heighten appetite, but this is not observed under the more common condition in which NNS is ingested in conjunction with other energy sources. Substitution of NNS for a nutritive sweetener generally elicits incomplete energy compensation, but evidence of long-term efficacy for weight management is not available. The addition of NNS to diets poses no benefit for weight loss or reduced weight gain without energy restriction. There are long-standing and recent concerns that inclusion of NNS in the diet promotes energy intake and contributes to obesity. Most of the purported mechanisms by which this occurs are not supported by the available evidence, although some warrant further consideration. Resolution of this important issue will require long-term randomized controlled trials.

 

[Calyptus]

http://www.ncbi.nlm.nih.gov/pubmed/12782208

Physiol Behav. 2003 Apr;78(4-5):557-62.
Physiological mechanisms mediating aspartame-induced satiety.
Hall WL, Millward DJ, Rogers PJ, Morgan LM.
Source

Centre for Nutrition and Food Safety, School of Biomedical and Life Sciences, University of Surrey, Guildford, Surrey GU2 7XH, UK. w.l.hall@reading.ac.uk
Abstract

Aspartame has been previously shown to increase satiety. This study aimed to investigate a possible role for the satiety hormones cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) in this effect. The effects of the constituents of aspartame, phenylalanine and aspartic acid, were also examined. Six subjects consumed an encapsulated preload consisting of either 400 mg aspartame, 176 mg aspartic acid+224 mg phenylalanine, or 400 mg corn flour (control), with 1.5 g paracetamol dissolved in 450 ml water to measure gastric emptying. A 1983-kJ liquid meal was consumed 60 min later. Plasma CCK, GLP-1, glucose-dependent insulinotropic polypeptide (GIP), glucose, and insulin were measured over 0-120 min. Gastric emptying was measured from 0 to 60 min. Plasma GLP-1 concentrations decreased following the liquid meal (60-120 min) after both the aspartame and amino acids preloads (control, 2096.9 pmol/l min; aspartame, 536.6 pmol/l min; amino acids, 861.8 pmol/l min; incremental area under the curve [AUC] 60-120 min, P<.05). Desire to eat was reduced from 60 to 120 min following the amino acids preload (control, -337.1 mm min; aspartame, -505.4 mm min; amino acids, -1497.1 mm min; incremental AUC 60-120 min, P<.05). However, gastric emptying rates, plasma CCK, GIP, insulin, and glucose concentrations were unaffected. There was a correlation between the increase in plasma phenylalanine and decrease in desire to eat after the liquid meal following the constituent amino acids (r=-.9774, P=.004). In conclusion, it is unlikely that aspartame increases satiety via CCK- or GLP-1-mediated mechanisms, but small changes in circulating phenylalanine concentrations may influence appetite.

Klik om te verkleinen...

die "may" slaagt op een verminderend effect op eetlust eh...

---------- Post toegevoegd Sat 26 Jan 2013 om 21:18 ----------

Resolution of this important issue will require long-term randomized controlled trials.

Klik om te verkleinen...

welk deel van dit abstract snap je niet

 

[houston]

Physiol Behav. 2010 Apr 26;100(1):55-62. doi: 10.1016/j.physbeh.2009.12.021. Epub 2010 Jan 6.
High-intensity sweeteners and energy balance.
http://www.ncbi.nlm.nih.gov/pubmed/20060008

Swithers SE, Martin AA, Davidson TL.
Source

Department of Psychological Sciences, Purdue University, 703 Third Street, West Lafayette, IN 47907, United States. swithers@purdue.edu
Abstract

Recent epidemiological evidence points to a link between a variety of negative health outcomes (e.g. metabolic syndrome, diabetes and cardiovascular disease) and the consumption of both calorically sweetened beverages and beverages sweetened with high-intensity, non-caloric sweeteners. Research on the possibility that non-nutritive sweeteners promote food intake, body weight gain, and metabolic disorders has been hindered by the lack of a physiologically-relevant model that describes the mechanistic basis for these outcomes. We have suggested that based on Pavlovian conditioning principles, consumption of non-nutritive sweeteners could result in sweet tastes no longer serving as consistent predictors of nutritive postingestive consequences. This dissociation between the sweet taste cues and the caloric consequences could lead to a decrease in the ability of sweet tastes to evoke physiological responses that serve to regulate energy balance. Using a rodent model, we have found that intake of foods or fluids containing non-nutritive sweeteners was accompanied by increased food intake, body weight gain, accumulation of body fat, and weaker caloric compensation, compared to consumption of foods and fluids containing glucose. Our research also provided evidence consistent with the hypothesis that these effects of consuming saccharin may be associated with a decrement in the ability of sweet taste to evoke thermic responses, and perhaps other physiological, cephalic phase, reflexes that are thought to help maintain energy balance.

Copyright 2010 Elsevier Inc. All rights reserved.

 

[Robjee]

Misschien het abstract nog eens goed lezen Houston...:

Aspartame has been previously shown to increase satiety. This study aimed to investigate a possible role for the satiety hormones cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) in this effect.

Klik om te verkleinen...

 

[houston]

die "may" slaagt op een verminderend effect op eetlust eh...

---------- Post toegevoegd Sat 26 Jan 2013 om 21:18 ----------



welk deel van dit abstract snap je niet

Klik om te verkleinen...

long-term randomized controlled trials zijn er al geweest.

 

[Galen]

Gaat over NNS i.h.a. we hadden het over aspartaam. Publicatie is van Purdue University en volgens je eigen beredenering dus ongeldig. Daarnaast wat Calyptus zegt en de auteurs vermelden:

Indeed, there is emerging evidence that selected NNS may stimulate the release of satiety hormones, although the link between these hormones and energy intake in free-living individuals is also open to debate.

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En satiety is nu precies waar deze discussie tevens om ging.

 

[Calyptus]

epidemiological evidence

wat een mooi woord voor correlatie.

 

[houston]

http://www.ncbi.nlm.nih.gov/pubmed/21424985

Q J Exp Psychol (Hove). 2011 Jul;64(7):1430-41. doi: 10.1080/17470218.2011.552729.
Intake of high-intensity sweeteners alters the ability of sweet taste to signal caloric consequences: implications for the learned control of energy and body weight regulation.
Davidson TL, Martin AA, Clark K, Swithers SE.
Source

Department of Psychological Sciences, Purdue University, West Lafayette, IN 47907, USA. tdavidso@purdue.edu
Abstract

Recent results from both human epidemiological and experimental studies with animals suggest that intake of noncaloric sweeteners may promote, rather than protect against, weight gain and other disturbances of energy regulation. However, without a viable mechanism to explain how consumption of noncaloric sweeteners can increase energy intake and body weight, the persuasiveness of such results has been limited. Using a rat model, the present research showed that intake of noncaloric sweeteners reduces the effectiveness of learned associations between sweet tastes and postingestive caloric outcomes (Experiment 1) and that interfering with this association may impair the ability of rats to regulate their intake of sweet, but not nonsweet, high-fat and high-calorie food (Experiment 2). The results support the hypothesis that consuming noncaloric sweeteners may promote excessive intake and body weight gain by weakening a predictive relationship between sweet taste and the caloric consequences of eating.

© 2011 The Experimental Psychology Society

 

[Galen]

epidemiological evidence

wat een mooi woord voor correlatie.

Klik om te verkleinen...

Kwam laatst overigens een boek tegen die jou wellicht bevalt.
http://www.amazon.com/Logically-Fallacious-Collection-Fallacies-ebook/dp/B007BYSM9Y

Heb hem voor als je wilt.

 

[houston]

http://www.ncbi.nlm.nih.gov/pubmed/23088901

Appetite. 2013 Jan;60(1):203-7. doi: 10.1016/j.appet.2012.10.009. Epub 2012 Oct 23.
Saccharin and aspartame, compared with sucrose, induce greater weight gain in adult Wistar rats, at similar total caloric intake levels.
Feijó Fde M, Ballard CR, Foletto KC, Batista BA, Neves AM, Ribeiro MF, Bertoluci MC.
Source

Programa de Pós-Graduação em Medicina: Ciências Médicas, Faculdade de Medicina da Universidade Federal do Rio Grande do Sul, Ramiro Barcelos 2400, CEP 90035-003, Porto Alegre, Brazil.
Abstract

It has been suggested that the use of nonnutritive sweeteners (NNSs) can lead to weight gain, but evidence regarding their real effect in body weight and satiety is still inconclusive. Using a rat model, the present study compares the effect of saccharin and aspartame to sucrose in body weight gain and in caloric intake. Twenty-nine male Wistar rats received plain yogurt sweetened with 20% sucrose, 0.3% sodium saccharin or 0.4% aspartame, in addition to chow and water ad libitum, while physical activity was restrained. Measurements of cumulative body weight gain, total caloric intake, caloric intake of chow and caloric intake of sweetened yogurt were performed weekly for 12 weeks. Results showed that addition of either saccharin or aspartame to yogurt resulted in increased weight gain compared to addition of sucrose, however total caloric intake was similar among groups. In conclusion, greater weight gain was promoted by the use of saccharin or aspartame, compared with sucrose, and this weight gain was unrelated to caloric intake. We speculate that a decrease in energy expenditure or increase in fluid retention might be involved.

Copyright © 2012 Elsevier Ltd. All rights reserved.

 

[Galen]

Publicatie is van Universidade Federal do Rio Grande do Sul en volgens je eigen beredenering dus ongeldig. En raad eens waarom ratten studies wat betreft eetgewoonten bizar slecht transleren naar mensen.

 

[Calyptus]

een ratstudie zonder controlgroup?

Zijn ze in Brazilië echt nog zo achterlijk?

 

[Robjee]

Houston, volgens mij zoek je selectief naar onderzoeken die jouw standpunt bevestigen. Hierbij verlies je de kwaliteit en bewijskracht van de onderzoeken uit het oog (je valt zelfs terug of dierproeven) en negeer je resultaten uit onderzoek (bij mensen) die jouw standpunt niet bevestigen.
Hoewel negereren... waarom haal je de onderzoeken van Mattes et al en Hall et al aan? Wat wil je hiermee zeggen?