Tuesday, December 23, 2025

the Reactive Oxidative Species and Free Fatty Acid damage from Ethanol/glucose/Fructose binging: Robert Lustig research...

 https://www.youtube.com/playlist?list=PLaxpujmz7Q05h-NGllwGaAzS5HcT6SS8s

on Alcohol as accelerating aging... from increased ATP production with Reactive Oxidative Species and Free Fatty Acids... 

 it's the fructose combined with the glucose - read Robert Lustig for the biochemical details. the fructose turns into Free Fatty Acids as DNL or De Novo Lipogenesis. Alcohol does the same - it's all based on dosage. So HFCS is synthetic sugar with no ezyme - so it's a fructose dump straight to the liver. Fruit has too much fiber so the fructose goes to the small intestines before the liver. If there is a binge of alcohol it also gets turned into fat and free radicals. So sugar is chronic poison and ethanol is acute poison.

   

 https://pmc.ncbi.nlm.nih.gov/articles/PMC8882865/

 Ginger is rich in polyphenols, primarily gingerols in fresh ginger, which transform into shogaols

 Conversely, if you are obese, insulin resistant, fed, and getting both fructose and glucose together (a sizable percentage of the population), then fructose gets converted to fat at a much higher rate, ∼30% ().............

 Although the absolute rate of DNL of ethanol (i.e., that which is metabolized to VLDL) is relatively small, fractional DNL increases from 1% at baseline to 31% after an ethanol bolus (); thus, the liver is primed to convert ethanol to FFAs.

 

 

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