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In terms of this particular piece of research, here is the Abstract:

The investigators are all from the Section of Endocrinology, Department of Internal Medicine, Yale University School of Medicine -- certainly people who know the science of what they're studying and thinking about.

Well, I'm not so sure about that! I think the study is fundamentally flawed and probably should not have been published without fundamental consideration of differences in the physiological/biochemical/metabolic properties of fructose vs. glucose.

Ingested fructose is cleared from the portal vein after absorption. The concentration of fructose in serum is less than 20 micromolar. I have seen no data to indicate how much, if any, the serum fructose concentration increases after ingestion of a fructose bolus. The fructose taken up by the liver is converted to F-1-P for metabolic pathways and I don't think "excess" fructose can be "dumped" back into the bloodstream (as is the case for glucose).

By contrast, glucose cleared from the portal vein by the liver is converted to G-6-P which can then be channeled into several metabolic pathways or dumped back into the bloodstream when the concentration in the liver exceeds metabolic demand.

Since the study in question measured hormonal and cerebral endpoints, how can they distinguish between the effects caused by glucose itself or (in the case of fructose ingestion) the lack of glucose and the metabolic consequences of ingesting large amounts of fructose in the absence of glucose?

I don't see how the cerebral differences can be attributed directly to fructose. They must be due to metabolic consequences of metabolism of fructose in the liver. However, since they apparently used 100% fructose in the absence of glucose, they are measuring an abnormal metabolic response. There really is no way to relate this to the normal state of ingesting a 50/50 mixture (sugar) or a 55/45 mixture (HFCS).

The problem with fundamentally flawed studies is that there is just no way to know what the results mean. For example, the ingestion of a bolus of fructose by itself, might lead to a temporary ATP depletion/deficit in the liver that signals hunger and stimulates eating. That may or may not occur when eating a bolus of HFCS.

They spent a lot of time and money doing experiments that probably don't have anything to do with their stated objective of relating the ingestion of HFCS to obesity and blaming it on the fructose. If they do their measurements using HFCS vs sucrose (and they probably did), they probably would not see any differences. If they do the experiment using HFCS vs glucose (and they probably did), they still might not see any differences. If they do the experiment using HFCS vs fructose (and they should have), they still might not see any differences.

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