Neurobiologisk påverkan och viktökning av kalorifria artificiella sötningsmedel

[King Grub]

Increasing evidence suggests that artificial sweeteners do not activate the food reward pathways in the same fashion as natural sweeteners. Lack of caloric contribution generally eliminates the postingestive component. Functional magnetic imaging in normal weight men showed that glucose ingestion resulted in a prolonged signal depression in the hypothalamus. This response was not observed with sucralose ingestion. Natural and artificial sweeteners also activate the gustatory branch differently. The sweet taste receptor, a heterodimer of two G protein coupled transmembrane receptors, contain several ligand-binding sites. For instance, aspartame and cyclamate, respectively, bind to each of the two monomers. On the functional level, sucrose ingestion, compared to saccharin ingestion, was associated with greater activation of the higher gustatory areas such as the insula, orbitofrontal cortex, and amygdala.

These pilot investigations are consistent with a revised hypothesis: Sweetness decoupled from caloric content offers partial, but not complete, activation of the food reward pathways. Activation of the hedonic component may contribute to increased appetite. Animals seek food to satisfy the inherent craving for sweetness, even in the absence of energy need. Lack of complete satisfaction, likely because of the failure to activate the postingestive component, further fuels the food seeking behavior. Reduction in reward response may contribute to obesity. Impaired activation of the mesolimbic pathways following milkshake ingestion was observed in obese adolescent girls.

Lastly, artificial sweeteners, precisely because they are sweet, encourage sugar craving and sugar dependence. Repeated exposure trains flavor preference. A strong correlation exists between a person’s customary intake of a flavor and his preferred intensity for that flavor. Systematic reduction of dietary salt or fat without any flavorful substitution over the course of several weeks led to a preference for lower levels of those nutrients in the research subjects. In light of these findings, a similar approach might be used to reduce sugar intake. Unsweetening the world’s diet may be the key to reversing the obesity epidemic.

Yale J Biol Med. 2010 Jun;83(2):101-8. Gain weight by "going diet?" Artificial sweeteners and the neurobiology of sugar cravings: Neuroscience 2010.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2892765/

[Crocker]

Positivt, mer coca cola zero! :)

[King Grub]

Texten var inte positiv till sötningsmedel, utan ansåg att sötningsmedel kan bidra till övervikt...

[Crocker]

Texten var inte positiv till sötningsmedel, utan ansåg att sötningsmedel kan bidra till övervikt...

Unsweetening the world’s diet may be the key to reversing the obesity epidemic.

Menar de sötningsmedel då eller?

[JoeyP]

Dem menar på att sötningsmedel kan ge ökad aptit. Man blir sugen på socker?

[King Grub]

Menar de sötningsmedel då eller?

Socker och sötningsmedel, ja.

[Crocker]

Socker och sötningsmedel, ja.
Ok, missförståelse.

[Pepz]

känns som detta pekar på att Sockerberoende(söt-beroende) faktiskt kan existera rent fysiologisk?

[mikaelj]

Är det inte konstaterat att socker ger ökad dopaminfrisättning?

[Anders The Peak]

känns som detta pekar på att Sockerberoende(söt-beroende) faktiskt kan existera rent fysiologisk?

Är det inte det studien/artikeln egentligen säger ...

[dt06mj2]

Jag kör dock bara sötningsmedel i alla söta saker jag äter. Har antagligen inte fått i mig mer än en halv dl socker senaste månaden. I beat the system!

[mikaelj]

Är det bara sött då? Många knarkar mackor...

Dessutom stod det glukos. Strösocker är bara hälften glukos. Medans stärkelse [bryts ned till] just glukos.

[Eddie Vedder]

känns som detta pekar på att Sockerberoende(söt-beroende) faktiskt kan existera rent fysiologisk?

Här är referens #41 från artikeln:

AbstractThe experimental question is whether or not sugar can be a substance of abuse and lead to a natural form of addiction. “Food addiction” seems plausible because brain pathways that evolved to respond to natural rewards are also activated by addictive drugs. Sugar is noteworthy as a substance that releases opioids and dopamine and thus might be expected to have addictive potential. This review summarizes evidence of sugar dependence in an animal model. Four components of addiction are analyzed. “Bingeing”, “withdrawal”, “craving” and cross-sensitization are each given operational definitions and demonstrated behaviorally with sugar bingeing as the reinforcer. These behaviors are then related to neurochemical changes in the brain that also occur with addictive drugs. Neural adaptations include changes in dopamine and opioid receptor binding, enkephalin mRNA expression and dopamine and acetylcholine release in the nucleus accumbens. The evidence supports the hypothesis that under certain circumstances rats can become sugar dependent. This may translate to some human conditions as suggested by the literature on eating disorders and obesity.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2235907/

Nicole M et al. Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008; 32(1): 20–39.

Referens #47:

Dopamine is known to regulate food intake by modulating food reward via the mesolimbic circuitry of the brain. The objective of this study was to compare the effects of high energy input (i.v. glucose) on striatal and thalamic dopamine release in overweight and lean individuals. We hypothesized that glucose would induce dopamine release and positive ratings (e.g., satiety) in Behavioral Analog Scales, particularly in food-deprived lean subjects. [(11)C]raclopride PET was performed for 12 lean (mean BMI = 22 kg/m(2)) and 12 overweight (mean BMI = 33 kg/m(2)) healthy subjects. Each subject was imaged twice in a blinded counter-balanced setting, after 300 mg/kg i.v. glucose and after i.v. placebo. Dopamine D2 receptor binding potentials (BPs) were estimated. The voxel-based analysis of the baseline scans indicated lower striatal BPs in the overweight group and a negative correlation between BMIs and BPs. Intravenous glucose did not have a significant effect on BPs in overweight or lean subjects (male and female groups combined). However, BP changes were opposite in the two gender groups. In male subjects, significant BP reductions after glucose were seen in the right and left caudate nucleus, left putamen, and right thalamus. In female subjects, increases in BP secondary to glucose were seen in the right caudate nucleus and right and left putamen. The sexually dimorphic effect of glucose was seen in both overweight and lean subjects. Although gender differences were not among the a priori hypotheses of the present study and, therefore, they must be considered to be preliminary findings, we postulate that this observation is a reflection of an interaction between glucose, sex steroids (estrogen), leptin, and dopamine.

http://www3.interscience.wiley.com/cgi-bin/fulltext/114278932/PDFSTART

Haltia LT et al. Effects of intravenous glucose on dopaminergic function in the human brain in vivo. Synapse. 2007 Sep;61(9):748-56.

[Ola Wallengren]

Har inte läst fullängdaren men vad de spekulerar kring saknar, så vitt jag vet, något större stöd i mycket av den forskningen som finns kring sötningsmedel på människa, nämligen att intag av sötningsmedel ökar intaget mer än intag av mostvarande sockersötad vara.

[Ola Wallengren]

Rekommenderar den har för lite annan syn på saken.

Clin Nutr. 2010 Jun;29(3):288-303. Epub 2009 Dec 28.

The plausibility of sugar addiction and its role in obesity and eating disorders.
Benton D.

Department of Psychology, University of Swansea, Swansea SA2 8PP, Wales, United Kingdom. d.benton@swansea.ac.uk

Abstract
BACKGROUND & AIMS: To consider the hypothesis that addiction to food, or more specifically sucrose, plays a role in obesity and eating disorders. METHODS: By considering the relevant literature a series of predictions were examined, derived from the hypothesis that addiction to sucrose consumption can develop. Fasting should increase food cravings, predominantly for sweet items; cravings should occur after an overnight fast; the obese should find sweetness particularly attractive; a high-sugar consumption should predispose to obesity. More specifically predictions based on the hypothesis that addiction to sugar is central to bingeing disorders were developed. Dieting should predate the development of bingeing; dietary style rather than psychological, social and economic factors should be predispose to eating disorders; sweet items should be preferentially consumed while bingeing; opioid antagonists should cause withdrawal symptoms; bingeing should develop at a younger age when there is a greater preference for sweetness. RESULTS: The above predications have in common that on no occasion was the behaviour predicted by an animal model of sucrose addiction supported by human studies. CONCLUSION: There is no support from the human literature for the hypothesis that sucrose may be physically addictive or that addiction to sugar plays a role in eating disorders. Copyright 2009 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.

[Musselbank]

Har inte läst fullängdaren men vad de spekulerar kring saknar, så vitt jag vet, något större stöd i mycket av den forskningen som finns kring sötningsmedel på människa, nämligen att intag av sötningsmedel ökar intaget mer än intag av mostvarande sockersötad vara.


Fast är det det de säger? Jag uppfattar det som att de bara mumlar om att sötma är problematisk även när den är icke-sockrig. Inte att sötningsmedel är värre än eller ens lika illa som socker.

[hejhopp79]

Positivt, mer coca cola zero! :)

Vad pratar du om LOL

[hejhopp79]

känns som detta pekar på att Sockerberoende(söt-beroende) faktiskt kan existera rent fysiologisk?

Allting som påverkar hjärnan och får oss att må bra kan skapa ett beroende, däribland socker.

[hejhopp79]

Är det inte konstaterat att socker ger ökad dopaminfrisättning?

Det gör det med all sannolikhet, eftersom stimulerande effekter oavsett ämne oftast handlar om ökad frisättning av dopamin och stresshormoner som noradrenalin/adrenalin.