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Fat emperor intervjuar professor Robert Lustig

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Enormt bra intervju massor med information !! Tack. 

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Lustig var den som fick mig in på det sockerfria spåret 2013. Inspirerande föreläsare!

Som någon kommenterade efter intervjun: "It's like the Super Bowl in nutrition."

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🤓 Från R Lustigs hemsida, https://robertlustig.com/fructose-restriction/

Isocaloric Fructose Restriction Reduces Serum D-Lactate Concentration in Children With Obesity and Metabolic Syndrome
The Journal of Clinical Endocrinology & Metabolism, 2019

  • Study shows that a fructose metabolite in the liver, methylglyoxal (of which Dlactate is the breakdown product), correlates with changes in both de novo lipogenesis and insulin resistance when starch is substituted for sugar. Short version: SUGAR IS TOXIC! And here’s the toxin.

 

🤓 Googlade methylglyoxal och fann en tidigare artikel av en av medförfattarna till ovanstående artikel:

Gugliucci A. (2017). Formation of Fructose-Mediated Advanced Glycation End Products and Their Roles in Metabolic and Inflammatory Diseases.
Advances in nutrition, 8(1), 54–62.

  • Fructose is associated with the biochemical alterations that promote the development of metabolic syndrome (MetS), nonalcoholic fatty liver disease, and type 2 diabetes. Its consumption has increased in parallel with MetS. It is metabolized by the liver, where it stimulates de novo lipogenesis. The triglycerides synthesized lead to hepatic insulin resistance and dyslipidemia. Fructose-derived advanced glycation end products (AGEs) may be involved via the Maillard reaction. /

 

  • .../  Fructose is elevated in several tissues of diabetic patients where the polyol pathway is active, reaching the same order of magnitude as glucose. It is plausible that the high reactivity of fructose, directly or via its metabolites, may contribute to the formation of intracellular AGEs and to vascular complications.

 

Allaman, I., Bélanger, M., & Magistretti, P. J. (2015). Methylglyoxal, the dark side of glycolysis. Frontiers in neuroscience, 9, 23.

  • Methylglyoxal, a highly reactive dicarbonyl compound, is inevitably formed as a by-product of glycolysis. Methylglyoxal is a major cell-permeant precursor of advanced glycation end-products (AGEs), which are associated with several pathologies including diabetes, aging and neurodegenerative diseases. In normal situations, cells are protected against methylglyoxal toxicity by different mechanisms and in particular the glyoxalase system, which represents the most important pathway for the detoxification of methylglyoxal.
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  • Tack! 2

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