----- "Geoffrey Purcell" <[log in to unmask]> wrote: 
> 
> We seem to be arguing for no reason, then if you're not against whole fruits. I stated that there were other substances within fruits that clearly negate the negative effects of fructose given the vast number of studies showing an overall health-benefit for diets high in fruit/veg(though not vegan ones) - (that is, unless there are studies clearly showing extreme damage to the liver as the proportion of fruits/veg increases). 

We're arguing because, when I mentioned studies that show that fructose causes NAFLD, you said the studies were meaningless. You didn't support that claim, and you still haven't done so. Even now, you are missing the point. I have been talking about NAFLD and its sequelae. In your previous post, you cited a study showing that citrus fruits, in particular, may have a protective effect against ischemic stroke. I pointed out that this is not relevant to the question of fructose and NAFLD. But now again, you say that there are "other substances within fruits that clearly negate the negative effects of fructose." It should be obvious that a study that shows that citrus fruits may protect against ischemic stroke doesn't show that fruits have substances that prevent them from contributing to NAFLD and its complications. 

> As for dosage levels, this page gives details, claiming less than 90g of fructose a day is fine:- 
> 
> http://www.ajcn.org/cgi/content/full/88/5/1189 

Very good. Did you bother to read the editorial before pasting the link? This editorial presents rather substantial arguments that are *critical* of the 90g ceiling hypothesis. "This meta-analysis is difficult to interpret, because it involves randomized and nonrandomized studies of differing designs, mixed populations (diabetic and nondiabetic, lean and obese), different control diets (including some sucrose-based diets that contained fructose), different study durations, and limited endpoints; it also represents an analysis by an industry-sponsored group of a highly selected list of studies (42 of 3331)." 

This editorial, in fact, rather forcefully states and documents a case *against* consumption of fructose at the 90g level. They even go so far as to assert that "a better index for cardiovascular risk may be a fructose index based on the percentage and amount of fructose in various foods ( 3 )." They conclude "In conclusion, obesity and diabetes rates were low when total fructose intake was in the range of 25–40 g/d. Conclusions as to the safe and prudent amounts of fructose consumption will require carefully controlled dose-responses studies in different populations, including subjects with metabolic syndrome who are at greater risk of diabetes and cardiovascular disease, rather than depending on meta-analyses of existing studies of mixed design and duration." 

I find this quite interesting, in that it converges with various studies of alcohol consumption. There have been many studies indicating that low to moderate alcohol consumption has a protective effect against cardiovascular disease. Not *all* studies show this, but many do. There's much debate about whether it's the alcohol itself, or something else (such as the resveratrol in red wine), but let's suppose, for the sake of argument, that it's the alcohol. The usual claim is that there is a "J curve" with respect to alcohol consumption and cardiovascular risk. That is, people who have one or two drinks a day have lower cardiovascular disease rates than abstainers, but people who consume any more that have increased risk, and the risk increases sharply as the amount of alcohol consumed increases--hence the J shape. Scientists have a precising definition of a "drink" as an ounce of spirits, or 6 ounces of wine, or 12 ounces of beer. In each case the amount of alcohol consumed is roughly 13 g. So, "two drinks" means 26 g of alcohol. Now, we also know that the metabolism of fructose is virtually identical to that of alcohol, in its effect on the liver. Both are immediately converted to triglyceride, both cause uric acid to increase, etc. A reasonably hypothesis is that fructose has the very same J curve of cardiovascular risk. This is consistent with the 25-40 g/d level mentioned in the editorial, allowing for substantial variation in body weight. But as the authors state, that's just a guess, requiring a lot more study. 

It would also make sense, for those people who also consume alcohol, to add the two together in calculating their exposure. Finally, as the editorial authors indicate, people who already have metabolic syndrome may need to limit fructose (and alcohol) intake more drastically. I suspect that this is the case. 

Am I "against whole fruits"? I don't even know what the hell that means. Whole fruits are, in my opinion, paleo. I'm pretty confident that when they were available, paleo ate them. Why wouldn't they? They provide energy and taste good. But I reject the inference that because paleo people ate whole fruits, they are entirely harmless. Moreover, I am increasingly convinced that the "threshold of harm" for fructose consumption is fairly low, especially when considering modern, cultivated fruits. It's very easy to go past 26g of fructose just eating grapes, apples, and pears. And for people who are already insulin resistant, 26 g may be 26 g too much. In short, because fructose and ethanol are so metabolically similar, I think they should be considered equivalent for purposes of deciding how much to consume. 

Todd Moody 
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