LONGECITY

Some vegetables are fine. But the whole 5 servings of fruit, or the longecity version 100 - 200 grams of blueberries / berries a day sounds like bullshit to me. Fruits are such a modern addition in large quantities to our diet, obviously they have fiber so they will have lower GI than straight up sucrose, but what about fructose and the liver. It fucks it up right. The liver then starts to get sluggish and fatty, making your whole body trash. Sure, maybe some people with genetic mutations can eat whole load of them and suffer no problems. I remember reading that anything above 30 grams of fructose a day is impossible to use by the body unless someone is an athelete / avid exerciser.

Even saturated fat, which is in it's own not too healthy, goes into turbon poison mode when paired with fruits / fructose.

Even cutting out the one banana and a few tomatoes I eat a day made tremendous difference to my health (namely lower fasting blood sugar, more energy, eye bags clearing up, etc.).

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.

There is not a "longecity version" of any way of eating, much less a specific berry amount. There are only some members opinions on all issues.