The anti-carb warrior dr. Lustig has come out with a new study demonstrating the toxicity of excess fructose. The results link the fructose metabolite methylglyoxal to liver stress, which results in insulin resistance through emergency DNL and ultimately metabolic syndrome. Methylglyoxal is 250 times more glycating than glucose.
This study also apparently supports the view that endotoxin is a key driver of metabolic syndrome, as D-lactate is produced by bacterial overgrowth while L-lactate is what humans produce. Maybe bad intestinal bacteria love to use fructose as food?
Isocaloric Fructose Restriction Reduces Serum D-Lactate Concentration in Children With Obesity and Metabolic Syndrome
This study also apparently supports the view that endotoxin is a key driver of metabolic syndrome, as D-lactate is produced by bacterial overgrowth while L-lactate is what humans produce. Maybe bad intestinal bacteria love to use fructose as food?
Isocaloric Fructose Restriction Reduces Serum D-Lactate Concentration in Children With Obesity and Metabolic Syndrome
Conclusion
Baseline correlation of D-lactate with DNL and measures of insulin sensitivity; and reduction in D-lactate following nine days of isocaloric fructose restriction suggest that DNL and non-enzymatic glycation are functionally linked via intermediary glycolysis in the pathogenesis of metabolic syndrome, and points to fructose as a key dietary substrate that drives both pathways.