They're by no means a modern addition. Berries are a huge part of the diet of the Hadza, who I find the best model for pre-agricultural hominin diets. Or you could consider the diets of our common ancestors with chimpanzees, bonobos, gorillas, gibbons, and old world monkeys.
Even Dr. Lustig would agree we're adapted to eating much of our calories from fruit, so long our livers aren't glycogen replete (ie, well-fed and sedentary). So, if you're concerned about fructose, have your servings of fruit upon waking (or otherwise breaking a fast), or after strenuous exercise.
In the hypercaloric glycogen-replete state, intermediary metabolites from fructose metabolism overwhelm hepatic mitochondrial capacity, which promotes de novo lipogenesis and leads to hepatic insulin resistance
Moreover, the polyphenols in berries and citrus fruit demonstrably oppose changes to the gut microbiome caused by the fructose/sucrose, and reduce uptake of lipopolysaccharide that appears to play a major role in the Kupffer cell inflammation that plays a major role in fatty liver. The also oppose inflammation throug NF-κB inhibition. Once in hepatocytes, they inhibit de novo lipogenesis and increase β-oxidation via AMPK activation.
Or you could look at the epidemiology. Whole fruit consumption is consistently associated with reduced incidence of diabetes, and higher polyphenol fruit appear to have a greater protective effect. However, fruit juice consumption, where sugar intake is higher at a sitting, and many of the polyphenols are discarded with the skins & pulp, is associated with increased incidence.
Marlowe and Berbesque, 2009. Tubers as fallback foods and their impact on Hadza hunter‐gatherers. Am J Phys Anthro, 140(4), pp.751-758.
Lustig, 2013. Fructose: it’s “alcohol without the buzz”. Adv Nut, 4(2), pp.226-235.
Mosele et al, 2015. Metabolic and microbial modulation of the large intestine ecosystem by non-absorbed diet phenolic compounds: a review. Molecules, 20(9), pp.17429-17468.
Valenti et al, 2013. Dietary anthocyanins as nutritional therapy for nonalcoholic fatty liver disease. Oxid med cell longevity, 2013.\
Rodriguez-Ramiro et al, 2016. Polyphenols and non-alcoholic fatty liver disease: impact and mechanisms. Proc Nut Soc, 75(1), pp.47-60.
Bazzano et al, 2008. Intake of fruit, vegetables, and fruit juices and risk of diabetes in women. Diabetes care, 31(7), pp.1311-1317
Muraki et al, 2013. Fruit consumption and risk of type 2 diabetes: results from three prospective longitudinal cohort studies. Bmj, 347, p.f5001.
Edited by Darryl, 22 November 2017 - 06:14 PM.
