I think that you have demonstrated sugar to be a player with the triglycerides, but there is no simple answer. There are many factors that go into metabolic syndrome and leptin resistance and they all make each other worse. We have here a plausible mechanism, but in the case of humans living their lives it is harder to say if it is all the sugar. We have a plausible mechanism but the important thing to note about metabolic syndrome is that there is no single cause, only many things that come together to aggravate it.

This is a great chart of dietary trends since the 70s. http://civileats.com/2011/04/05/where-do-americans-get-their-calories-infographic/

Sugar hasn't really gone up much, grains have gone up and "added fat" (seed oils) have skyrocketed. I think that sugar was probably a big contributor to obesity in the 70s, and it is a factor in itself when people get a whopping 450 calories from it in a day, but the seed oils and wheaty grain "products" also have plausible mechanisms to suggest that they are big players.

you'll have to pry my lindt from my cold dead hands!!!

but seriously, that's good stuff. i've been reading up on excessive fructose and it's effects on triglycerides also and this sounds very plausible.

I would suspect that uric acid reduction would not have the same effect in humans.

If gout medication led to weight loss, one would think that that effect would have been noticed, and even recorded in gout clinical trials. Actually, one possible side effect of the uric acid reducer allopurinol is weight gain. So things may be more complex.

One explanation for this might be that eating in humans differs from lab feeding in rats in two major ways: we are humans with different physiology, and we are free to eat what we want.

In addition, some randomized trials have shown greater weight loss with fructose-containing diets compared to low-fructose diets:

http://www.bodyrecomposition.com/research-review/the-effect-of-two-energy-restricted-diets-a-low-fructose-diet-vs-a-moderate-natural-fructose-diet-research-review.html

Unfortunately you can show that same association for a host of other variables too: calorie consumption, economic inequality, PUFA consumption, wheat consumption, processed food consumption and so on... (I even saw one linking niacin to the post-70s obesity epidemic). No wonder people just wave their hand at the whole of "the industrial lifestyle."

As to the fructose disturbing leptin point. Yes, this is important to remember, but I don't think it's a plausible candidate for the obesity epidemic. The disruption of leptin (and also ghrelin if I recall correctly, I've talked about both on here before) is temporary, so you would expect mere hours after a fructose meal leptin sensitivity would return. Although I can see why fructose could cause weight gain to a moderate extent, one would think that obese people, after a suitable period without fructose would have a crushing lack of appetite. This also doesn't seem to make sense of people eating large quantities of starch and fat, which seems common.

Edit:

So Travis makes a good point, which I'd completely missed, namely that fructose increases fasting as well as post-prandial triglycerides. Presumably this is why he suggests only in men and post-menopausal women, because the paper only shows a difference from fructose vs glucose feeding in men. On its own, this makes me suspicious that this is a dominant mechanism- it would be odd if men and women have both gotten obese, but through independent mechanisms.

Having looked at table 3, I find it a bit mysterious that both groups have declining triacylglycerols throughout. Also interesting is that the glucose men, after 7 days, have fasting levels significantly below baseline for their group.

The men started at 1.325mmol/L- after a week the fructose group were minimally higher at 1.34 (the highest they got and had lower levels than baseline every week thereafter), whereas the glucose group after a week are on 1.11mmol/L significantly below baseline levels, and they decrease pretty steadily throughout the study.

A quick and neat explanation for why this is the case might be that the men were consuming lots of fructose prior to the study, at baseline and so the fructose group more or less remained where they were (or, in fact, consumed a little less fructose and improved) whereas the enforced glucose/low fructose group steadily improved. But this seems somewhat unlikely since the fructose group were eating 17% of calories from fructose, whereas the study cites average intake as 9% (in 1988, it's increased a bit since then, but not that much, since fructose intake has only increased 19% since 1970.

I have been a sugar junkie since I was a little kid and it is still my biggest issue in transitioning my diet to a paleo/primal one and attempting to lose the 40-50 extra lbs that I am carrying. BUT, my trigs have consistently been under 70 for the last 10yrs or so at least and are currently sitting at 45.

So, either I am an outlier or there are other factors involved like some have suggested.

I don't think it is any one thing or any 3 ingredients all by themselves. If it were just sugar for example that was causing widespread obesity and disease, then simply cutting out sugar would cause widespread weight loss and health improvements, which it doesn't. Cutting out sugar is a good thing in general, but all by itself won't make you lose 50 pounds.

My personal opinion is that beer itself isn't a major contributor to obesity, but many of the things that go along with it are (sitting on the couch and watching tv, eating chips and wings, etc), i.e. the "beer lifestyle" contributes towards these problems, but beer itself is pretty low on the offender list. Sugary drinks for example I think are much worse.

I think bread and related "processed grain products" are a major factor for the subset of the population that is sensitive to gluten, which I think is a bigger subset than many people think.

The bad oils and fats also I think are a problem, but all by themselves don't really explain everything.

More than any of these things, I think it is the broad trend towards food that is highly processed and lacking in nutrition that is "the problem". These foods are high in all of these things, and also cause people to avoid eating "real" food.

The best all-encompassing explanation I've heard is the "insulin response" theory, which I think is likely correct or close enough to being correct. Also the theory that most problems are the result of inflammation, and thus indirectly by things that cause inflammation. You could probably come up with some trend charts over the past 50-70 years that show massive increases in foods and activities that exacerbate this basic problem.

This is very interesting to me for two reasons.

1, I have had a bit of an issue with dried fruits lately. I love them but then figured that was because it gave me my sugar fix and I could kid myself that 'cos they were fruit they were healthy. Of course I know this isn't the case and while dried fruits in moderation are OK, (I hope) the fructose in them is something that we should try and stay away from. While I've been told this by quite a few people, seeing it in this way really does prove what I have had niggling at the back of my brain for a few weeks.

2, I can use it to shut up all the people at work who think I'm a weirdo for not eating one of the doughnuts they brought in. :)

Thanks for posting it!

Paul.

The graph is a nightmare, cobbling together relatively unrelated data from several sources, and it is trying to get the untrained eye to be convinced of some sort of correlation. It should be ignored. In addition, the information is based on studies of men, and I fail to see how that would automatically apply to post-menopausal women. That said, there might still be something to your theory, or at least account for some of the increases in obesity. I know it is has not much to do in my case, as I ate an exemplary vegetarian whole-grain diet for many years before I became obese.

Sorry, I don't actually have an answer for you but could you supply the reference for the graph you posted please, I can't seem to find it (sorry if I'm being stupid)