Draft Notice: This section is still in draft form (yes, I write extemporaneously straight into "the cloud"). Links and references will follow.
I read the medical and basic science research in obesity pretty avidly and to my reading these are the five most important areas of basic science relating to obesity today (2012). Before I give the list let me clarify a few matters. I do not mean to suggest that these are the areas of research that are most likely to pay-off soon. Nor do I believe that these are the areas of research that are the most likely to pay off ever. I do however believe that these are questions that have the greatest potential to reshape our understanding of what obesity is and of what causes obesity. These are the (mostly) controversial theories that are not yet totally proven and are not demonstrably crazy. Many of these theories have one or a handful of brilliant scientist-clinicians who have made their theories their "raison d'etre". None of these theories is crackpot and not a one of them (except inflammation) is totally solid, unquestioned mainstream medicine or science. These are the "big-picture" theories that will either fall flat on their face or one day change the way we see the world.
In order to talk (or write) fairly about the role of fructose in obesity, one must, I must, at the outset acknowledge the pioneering work of Dr. Robert Lustig at the University of California at San Francisco. If one reads Lustig's considerable case against fructose, it is very compelling and he cites some very solid science. It is also important to know that Lustig's theories threaten some VERY powerful corporate interests in the United States and around the world and that these interests have the means (and perhaps the desire) to publicly smear him. Judging from the number of hateful anti-Lustig blogs that I have run across on the web, I confess to harboring at least some suspicion that "Big-Agra" may wish to silence him.
But is he right? Is fructose a metabolic "poison" to humans that can lead to obesity via leptin and insulin resistance? Well, in fairness, the science is split. Some research suggests that Lustig is right and other research "merely" demonstrates that sugar of any sort is as bad as sugar of any other sort. The REAL question is this: is fructose, calorie-for-calorie WORSE than glucose? Does fructose, because of its chemical structure, "poison" the body's ability to regulate adipose tissue (body fat) normally? For my part, I side with Lustig, but weakly. More good science is needed.
The relationship between obesity and chronic inflammation isn't even a theory, but is a scientifically validated fact and an important and central mechanism for many of the major medical consequences of obesity; above all, metabolic syndrome. I'll spend a lot more time talking about inflammation and obesity in sections of this website that cover metabolic syndrome, but for now here are the relevant points:
Closely tied to the subject of inflammation and obesity is the relationship between gut bacteria and obesity. It turns out that the bacteria that inhabit the human colon aren't merely "passengers" on (or in) the human body but are instead complex symbionts (beneficial parasites) that, among other things regulate immune function in mammals by carefully controlling the sorts of proteins (antigens) that gut is exposed to. This function happens normally when a certain balance of two major phyla (essentially basic types) of bacteria is properly maintained. Obesity can cause this balance to go awry and, when that happens, it feeds forward to induce further obesity. At least one of the major mechanisms for this 'vicious cycle' is chronic inflammation. Interestingly, there is also some question whether some kinds of gut bacteria may actually burn calories that would otherwise be absorbed from the colon (not the 'classical' site of calorie absorption). In other words, there is good evidence that normal poop keeps you thin and abnormal poop makes you fat (forgive the very 'plain' English).
Is obesity an infectious disease?
Probably not, but it is possible that obesity, at least in some cases, is caused, at least in part, by infectious agents, perhaps a virus? Maybe.
The evidence for this hypothesis is strongest with a human adenovirus called AD-36 which is indeed linked to obesity in children. Of course lots of things in the world are "linked" but that doesn't necessarily mean that one caused the other and that remains the weakness of the "infectobesity" hypothesis. Is AD-36 linked to obesity because it causes obesity or are kids who are prone, perhaps genetically, to become obese also more prone to become infected with AD-36?
It isn't clear.
It's tempting to dismiss infectobesity as an illusion or mere correlation but, the same was once said of a possible relationship between viruses and cancer. As you may know, it is now an absolute scientific certainty that some viruses can and do cause cancer. I wouldn't bet against a caussal relationship between viruses and obesity. Not yet anyway. A lot more science is needed.
Twenty years ago I dismissed talk of obesity caused by "chemicals and pollutants" as crackpot nonsense. I am now pretty sure that was arrogant and very 'young' of me. The fact is that today at least, there is some really good science showing that it is plausible and possible that chemicals produced as by-products of industrial civilization may play a role, even a big role in causing obesity.